Trauma Anesthesia

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Author: Charles Smith

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T R AU MA A N E S T H E S IA Injuries are estimated to become the number-one cause of death for men and women under the age of 45 by the year 2020. Trauma patients present unique challenges to anesthesiologists. Acute injuries require resource-intensive care and are often complex cases, especially when coupled with underlying, preexisting medical conditions. Anesthesiologists are involved with trauma patients beginning with airway and shock resuscitation, continuing with intraoperative care during surgery, and extending on to pain management and critical care postoperatively. This new reference focuses on a broad spectrum of traumatic injuries and the procedures anesthesiologists perform to adequately care for trauma patients perioperatively, surgically, and postoperatively. Special emphasis is given to the assessment and treatment of coexisting disease. Numerous tables and more than 300 illustrations showcasing various techniques of airway management, shock resuscitation, echocardiography, and use of ultrasound for the performance of regional anesthesia in trauma provide an invaluable reference for the anesthesiologist. Dr. Charles E. Smith is board-certified in anesthesiology and in perioperative transesophageal echocardiography, has expertise in trauma care, and has published extensively on topics in trauma anesthesia.

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T R AU M A A N E S T H E S I A

Edited by

C HA R L E S E . S M I T H MetroHealth Medical Center

Associate Editor

JOHN J. C OMO MetroHealth Medical Center

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CAMBRIDGE UNIVERSITY PRESS

Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press The Edinburgh Building, Cambridge CB2 8RU, UK Published in the United States of America by Cambridge University Press, New York www.cambridge.org Information on this title: www.cambridge.org/9780521870580 © Charles E. Smith 2008 This publication is in copyright. Subject to statutory exception and to the provision of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published in print format 2008

ISBN-13 978-0-511-41388-9

eBook (EBL)

ISBN-13

hardback

978-0-521-87058-0

Cambridge University Press has no responsibility for the persistence or accuracy of urls for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this publication to provide accurate and up-todate information that is in accord with accepted standards and practice at the time of publication. Nevertheless, the authors, editors, and publisher can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publisher therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this publication. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

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CONTENTS

Foreword: Adolph H. (Buddy) Giesecke, MD [Anesthesia] Foreword: Mark A. Malangoni, MD [Surgery] Preface Acknowledgments Contributors

1. Mechanisms and Demographics in Trauma Pedro Barbieri, Daniel H. Gomez, Peter F. Mahoney, Pablo Pratesi, and Christopher M. Grande 2. Trauma Airway Management William C. Wilson 3. Shock Management Richard P. Dutton 4. Establishing Vascular Access in the Trauma Patient Matthew A. Joy, Donn Marciniak, and Kasia Petelenz-Rubin 5. Monitoring the Trauma Patient Elizabeth A. Steele, P. David Søran, Donn Marciniak, and Charles E. Smith 6. Fluid and Blood Therapy in Trauma Maxim Novikov, and Charles E. Smith 7. Massive Transfusion Protocols in Trauma Care John E. Forestner 8. Blood Loss: Does It Change My Intravenous Anesthetic? Ken Johnson, and Talmage D. Egan 9. Pharmacology of Neuromuscular Blocking Agents and Their Reversal in Trauma Patients Fran¸cois Donati 10. Anesthesia Considerations for Abdominal Trauma William C. Wilson 11. Head Trauma – Anesthesia Considerations and Management Paul Tenenbein, M. Sean Kincaid, and Arthur M. Lam 12. Intensive Care Unit Management of Pediatric Brain Injury Robert Cohn, Maroun J. Mhanna, Elie Rizkala, and Dennis M. Super 13. Surgical Considerations for Spinal Cord Trauma Timothy Moore 14. Anesthesia for Spinal Cord Trauma M. Sean Kincaid, and Arthur M. Lam 15. Musculoskeletal Trauma Heather A. Vallier, and Mark D. Jenkins

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CONTENTS

16. Anesthetic Considerations for Orthopedic Trauma Robert M. Donatiello, Andrew D. Rosenberg, and Charles E. Smith 17. Cardiac and Great Vessel Trauma Naz Bige Aydin, Michael C. Moon, and Inderjit Gill 18. Anesthesia Considerations for Cardiothoracic Trauma Mark A. Gerhardt and Glenn P. Gravlee 19. Intraoperative One-Lung Ventilation for Trauma Anesthesia George W. Kanellakos and Peter Slinger 20. Burn Injuries (Critical Care in Severe Burn Injury) Charles J. Yowler 21. Anesthesia for Burns Jessica Anne Lovich-Sapola 22. Field Anesthesia and Military Injury Peter F. Mahoney and Craig C. McFarland 23. Eye Trauma and Anesthesia Martin Dauber and Steven Roth 24. Pediatric Trauma and Anesthesia Jocelyn Loy 25. Trauma in the Elderly Jeffrey H. Silverstein 26. Trauma in Pregnancy John R. Fisgus, Kalpana Tyagaraj, and Sohail Kamran Mahboobi 27. Oral and Maxillofacial Trauma Ketan P. Parekh and Cecil S. Ash 28. Damage Control in Severe Trauma Michael J. A. Parr and Ulrike Buehner 29. Hypothermia in Trauma Eldar Søreide and Charles E. Smith 30. ITACCS Management of Mechanical Ventilation in Critically Injured Patients Maureen McCunn, Anne J. Sutcliffe, Walter Mauritz, and the International Trauma Anesthesia and Critical Care Society (ITACCS) Critical Care Committee 31. Trauma and Regional Anesthesia Shalini Dhir and Sugantha Ganapathy 32. Ultrasound Procedures in Trauma Paul Soeding and Peter Hebbard 33. Use of Echocardiography and Ultrasound in Trauma Colin Royse and Alistair Royse 34. Pharmacologic Management of Acute Pain in Trauma Shalini Dhir, Veerabadran Velayutham, and Sugantha Ganapathy 35. Posttrauma Chronic Pain David Ryan and Kutaibba Tabbaa 36. Trauma Systems, Triage, and Transfer John J. Como 37. Teams, Team Training, and the Role of Simulation in Trauma Training and Management Paul Barach

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Index Color plates follow page

591 294

260 279 300 314 322 343 360 367 391 402 417 431 445 465

471 499 514 528 544 569

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F O R E WO R D

Dr. Charles E. Smith has been inspiring improved anesthesia for the victims of traumatic injury for many years, having spent the majority of his career at MetroHealth Medical Center, Cleveland, Ohio, which is the city’s major trauma center. He has regularly served as lecturer in refresher courses for the International Trauma Anesthesia and Critical Care Society (now called International TraumaCare). He is a productive author of innovative research in the care of the traumatized patient. These attributes easily qualify him to be editor of a multi-authored comprehensive book on trauma anesthesia, to which he is also a major contributor. His invited chapter authors are similarly qualified. The result is an authoritative, readable, and educational resource for the student, resident, or practitioner wishing to stay abreast of a rapidly changing field. Epochal changes have occurred in the practice of anesthesiology in the last ten years. Improved monitors, safer drugs, and better-trained anesthesiologists, nurse anesthetists, and anesthesia assistants have all reduced the morbidity and mortality of anesthesia. Anesthesia has become safer. Safer anesthesia improves the outcome of traumatic injuries. Our surgical colleagues have contributed to the improvements in trauma care. Innovations in the care of serious fractures, use of damage control in abdominal injuries, and improved care of burns have reduced morbidity and mortality. Dr. Smith has included all of the latest innovations in this text. Despite the advances, the importance of trauma as a cause of disability and lost life remains and, in fact, when expressed as a proportion to overall mortality in young people, is increasing in importance. Throughout history significant advances have been made in anesthetic care during times of war. The war in Iraq is no exception, and the lessons learned in that conflict are included. The technology of vascular access has greatly improved. Ultrasonic localization of major veins for central access is a major advance greatly enhancing safety for the patient. The technique of intraosseous infusion was once painful and cumbersome to establish, such that it was considered a circus stunt and not of much practical value. Newly designed equipment has revolutionized the technique. It is now fast, painless, convenient, and effective in any patient with difficult IV access. Having established vascular access, the choice and volume of fluid therapy is critical to survival and outcome of the

traumatized patient. This book discusses the established and the controversial concepts. Also discussed is a new protocoldriven, multidisciplinary approach to massive transfusion. This approach, which requires cooperation between the blood bank, the trauma surgeons, and anesthesiologists, takes the guesswork out of massive transfusion. No longer do we have to stand at the OR table and ponder, “Is it time for platelets and fresh frozen plasma?” These collaborative decisions have been made in advance, and all we have to do is to activate the protocol and administer whatever comes in the incremental allotments. Patients now expect to be relieved of significant pain, and pain is considered the fifth vital sign. Significant advances have been made in the techniques for relief of acute traumatic and postoperative pain. Entire teams of people are now dedicated to this practice. Nobody questions the value of pain relief, but it comes with some risk. A multimodal approach appears to accomplish the goal and simultaneously minimize the risks. Thermal injuries, brain injuries, and spinal cord injuries are specialized forms of trauma that are occasionally neglected. Not so in this text. The public health implications are presented along with the practical considerations for safe clinical management. The practical considerations are important because, for example, drugs and procedures that may be beneficial in the management of orthopedic injuries are contraindicated in neurologic injuries. We must be able to recognize these conflicts when they occur together in the same patient and create an anesthetic plan that will benefit the patient. Dr. Smith and his invited authors have done a magnificent job of pulling together the diverse concepts of the management of the traumatized patient and presenting us with a valuable resource for the anesthesiologist. Although directed at the anesthesiologist, the text is useful for emergency medicine physicians, surgeons, orthopedists, and, in fact, any health care professional who deals with trauma. Congratulations to the entire group of authors! Adolph H. (Buddy) Giesecke MD, Emeritus Professor Anesthesiology and Pain Management University of Texas Southwestern Medical Center Dallas, Texas

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F O R E WO R D

The challenge of managing seriously injured patients encompasses an expanse of issues linked by a common factor – trauma. In these critical situations, anesthesiologists are often faced with the need to simultaneously address emergent airway management, resuscitation, massive blood loss, acidemia, coagulopathy, hypothermia, and the consequences of damage to various organs. The management of each of these conditions alone can be essential for survival, and their convergence presents a unique situation in which the likelihood of death or a bad outcome is real. Success in this stressful situation requires a sophisticated understanding of basic sciences and expertise in the clinical and technical skills of anesthetic management. Together, the anesthesiologist and trauma surgeon must orchestrate the human and physical resources of the trauma center with a patient’s life on the line. Recent advances in the field of trauma anesthesiology parallel those in other related medical disciplines. Concepts promulgated by experiences in recent military conflicts have affected resuscitation and the use of blood products. The adoption of damage control operations and the use of simultaneous surgical teams to address multiple critical injuries have improved survival. Rules regarding the transfusion of blood and blood components and the use of recombinant clotting factors such as Factor VII concentrate have led to a “sea change” in trauma management that has resulted in the survival of soldiers and others injured under war conditions beyond what was possible just a few years ago. These concepts have been readily adopted in civilian trauma centers. The intensity associated with their

use has placed an increased demand on anesthesiologists who are already taxed in their care for the critically injured. This excellent book addresses these important and evolving changes in management of the injured patient as well as more traditional issues in trauma anesthesia. The breadth of topics addressed by the authors reflects the challenges and complexities of anesthesia-related care for victims of traumatic injury. Trauma surgeons realize the tremendous importance of coordinated care promulgated at trauma centers and by trauma systems. Injury accounts for more lost productive years of life than any other disease; therefore, survival and ultimate return to an acceptable level of function are important outcome parameters both for the patient, their loved ones, and our society. Because many seriously injured patients will require an operation, the anesthesiologist is an important link in the coordinated approach to trauma care and must be aware of the unique problems related to managing injury. That is why this book is such an important contribution for anesthesiologists who care for trauma patients. Mark A. Malangoni, MD Surgeon-in-Chief Chairperson, Department of Surgery MetroHealth Medical Center Professor of Surgery Case Western Reserve University School of Medicine Cleveland, Ohio

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P R E FAC E

Trauma is a leading cause of death and disability in modern society. Trauma will continue to be a leading cause of death well into the future. We are all vulnerable to traumatic injury. Managing adult and pediatric victims of major trauma and burns continues to be a great challenge requiring a tremendous amount of dedication and resources. The overall aim of this book is to review the anesthesia considerations for trauma patients and to provide a rational approach to choice of anesthetic techniques and drugs for injured patients. To accomplish this, I have assembled an outstanding group of clinicians who regularly care for trauma patients at major trauma centers. Each of them was asked to contribute a chapter that would provide an in-depth discussion on their area of expertise and that would concentrate on clinical aspects of trauma management. I have selected members of my hospital to assist with this textbook, as well as notable contributors from other major centers around the globe. The book consists of thirty-seven chapters that deal in detail with pertinent areas of trauma care, such as airway and shock management, monitoring, vascular access, pharmacology of anesthetic drugs, fluid and blood resuscitation, and the treatment of acute and chronic pain after injury. For several pat-

terns of injuries, including extremity and pelvis, spinal cord, burns, cardiac and great vessel, surgical considerations and management principles are presented to the reader in the chapter preceding the one dealing with anesthesia considerations. Specific chapters review the anesthesia considerations of vulnerable patient populations such as elderly, pediatric, pregnant, and military patients. Other sections deal with important issues of trauma care, including damage control in severe trauma, hypothermia in trauma, mechanical ventilation in critically injured patients, and use of echocardiography and ultrasound in trauma. Training for trauma, including the use of simulation and the role of trauma care systems in facilitating the allocation of resources for optimally managing injured patients are also covered. I hope that this book will be of use for anesthesia care providers who are faced with caring for trauma patients at all hours of the day and night. I am certain that the text will benefit anesthesia residents and staff of major trauma centers, help pave the way to improved care of the injured, and stimulate future advances in trauma care. Charles E. Smith, MD, FRCPC

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AC K N OW L E D G M E N T S

I would like to thank my mentors in anesthesia from McGill University – Drs. David Bevan, François Donati, and Earl Wynands – for providing teaching and inspiration, instilling in me the confidence to manage complex patients, and stimulating my interest in clinical research. I am indebted to all the staff at MetroHealth Medical Center who work long and hard to transport, stabilize, diagnose, treat, and rehabilitate victims of blunt and penetrating injury. Thanks to my associate editor, John Como, and to the many contributors to this book for sharing their experience and knowledge. I am grateful to Marc Strauss of Cambridge University Press, who first approached me with the formidable task of organizing this book, and to

Peg Brady for her tireless secretarial assistance. Appreciation goes to Peggy Rote, Monica Finley, Angela Weaver, Frank Scott, and the staff at Cambridge for their efforts in seeing this book through to publication. I would also like to thank my colleagues at the International Trauma Anesthesia and Critical Care Society (ITACCS, now called International TraumaCare) who have been a source of strength and guidance, in particular, Chris Grande, Buddy Giesecke, John Stene, and Eldar Søreide for their friendship and support. The love and encouragement of my parents, my wife, Bobby, and my children, Adrienne, Emily, and Rebecca, was ever present and much appreciated. Charles E. Smith, MD, FRCPC

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C ONTRIBUTORS

C E C I L S. A S H , DDS, MS Department of Oral and Maxillofacial Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio N A Z B I G E AY D I N , MD Department of Cardiothoracic Surgery, Cleveland Clinic, Cleveland, Ohio PAU L B A R AC H , MD, MPH Maj (ret.) Department of Anesthesia and Emergency Medicine, Utrecht University Medical Center, Utrecht, Netherlands P E D RO B A R B I E R I , MD Department of Anesthesia, Hospital Britanico de Buenos Aires, University of El Salvador School of Medicine, Buenos Aires, Argentina U L R I K E B U E H N E R , MD FCARCSI Anesthetic Department, St James’s University Hospital, Leeds, United Kingdom R O B E RT C O H N , MD Department of Pediatrics, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio J O H N J. C O M O , MD Department of Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio M A RT I N D AU B E R , MD Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois S HA L I N I D H I R , MD Department of Anesthesia and Perioperative Medicine, University of Western Ontario, London, Ontario, Canada F R A N Ç O I S D O NAT I , P H D, MD, FRCPC Department of Anesthesiology, Hôpital Maisonneuve-Rosemont, Université de Montréal, Montréal, Quebec, Canada

TA L MAG E D. E G A N , MD Department of Anesthesiology, University of Utah School of Medicine, Salt Lake City, Utah J O H N R. F I S G U S , MD Department of Anesthesia, Maimonides Medical Center, New York, New York J O H N E. F O R E S T N E R , MD Department of Anesthesiology and Pain Management, Parkland Memorial Hospital, University of Texas Southwestern Medical School, Dallas, Texas S U G A N T HA G A NA PAT H Y, MD, FRCA, FRCPC Department of Anesthesia and Perioperative Medicine, University of Western Ontario, London, Ontario, Canada M A R K A. G E R HA R D T, MD, P H D Department of Anesthesiology, Ohio State University Medical Center, Columbus, Ohio A D O L P H H. (B U D DY ) G I E S E C K E , MD Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical School, Dallas, Texas I N D E R J I T G I L L , MD Department of Cardiothoracic Surgery, Cleveland Clinic, Cleveland, Ohio D A N I E L H. G O M E Z , MD Department of Anesthesia, Hospital Universitario Austral, Pilar, Buenos Aires, Argentina C H R I S TO P H E R M. G R A N D E MD, MPH Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, and International TraumaCare (ITACCS), Baltimore, Maryland G L E N N P. G R AV L E E , MD Department of Anesthesiology, University of Colorado Health Sciences Center, Denver, Colorado

R O B E RT M. D O NAT I E L LO , MD Department of Anesthesiology, Hospital for Joint Diseases and Orthopedic Surgery, New York University Medical Center, New York, New York

P E T E R H E B BA R D , MBBS, FANZCA Department of Anaesthesia and Pain Management, Department of Pharmacology, Northeast Health Wangaratta, School of Rural Health University, Melbourne, Victoria, Australia

R I C HA R D P. D U T TO N , MD, MBA Division of Trauma Anesthesiology, R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore, Maryland

M A R K D. J E N K I N S , MD Department of Orthopedic Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio xv

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CONTRIBUTORS

K E N J O H N S O N , MD Department of Anesthesiology, University of Utah School of Medicine, Salt Lake City, Utah M AT T H E W A. J OY, MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio G E O RG E W. K A N E L L A KO S , MD, FRCPC Department of Anesthesia, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada M. S E A N K I N CA I D , MD Department of Anesthesiology, Harborview Medical Center, University of Washington Medical Center, Seattle, Washington A RT H U R M. L A M , MD, FRCPC Department of Anesthesiology, Harborview Medical Center, University of Washington Medical Center, Seattle, Washington J E S S I CA A N N E L OV I C H -S A P O L A , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio J OYC E LY N L OY, MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio S O HA I L K A M R A N M A H B O O B I , MD Department of Anesthesia, Maimonides Medical Center, New York, New York P E T E R F. M A H O N E Y, MD MS C , MBBS, FRCA, FFARCSI, FIMCRCSE D Military Critical Care, Royal Centre for Defence Medicine, Birmingham, United Kingdom M A R K A. M A L A N G O N I , MD Department of Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio D O N N M A RC I N IA K , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

T I M OT H Y M O O R E , MD Department of Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio M A X I M N OV I KOV, MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio K E TA N P. PA R E K H , DDS Department of Oral and Maxillofacial Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio M I C HA E L J. A. PA R R , MBBS, FRCP, FRCA, FANZCA, FJFICM Department of Intensive Care, Liverpool Hospital, University of New South Wales, Sydney, Australia K A S IA P E T E L E N Z -R U B I N , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio PA B LO P R AT E S I , MD Department of Emergency Medicine, Austral University Hospital, Pilar, Buenos Aires, Argentina E L I E R I Z KA L A , MD Department of Pediatrics, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio A N D R E W D. R O S E N B E RG , MD Department of Anesthesiology, Hospital for Joint Diseases and Orthopedic Surgery, New York University Medical Center, New York, New York S T E V E N R OT H , MD Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois A L I S TA I R R OYS E , MBBS, MD, FRACS Department of Anaesthesia and Pain Management, Department of Pharmacology, Royal Melbourne Hospital, University of Melbourne, Carlton, Victoria, Australia

WA LT E R M AU R I T Z , MD, P H D Department of Anesthesiology and Intensive Care, Trauma Hospital Lorenz Bohler, Vienna, Austria

C O L I N R OYS E , MBBS, MD, FANZCA Department of Anaesthesia and Pain Management, Department of Pharmacology, Royal Melbourne Hospital, University of Melbourne, Carlton, Victoria, Australia

M AU R E E N M C C U N N , MD, MIPP, FCCM Department of Anesthesia and Critical Care, Division of Trauma Anesthesiology, R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center, Baltimore, Maryland

D AV I D R YA N , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

C R A I G C. M C F A R L A N D , MD, MAJ, MC, FS Department of Anesthesiology, Uniformed Services, University of the Health Sciences, Bethesda, Maryland M A RO U N J. M HA N NA , MD Department of Pediatrics, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio M I C HA E L C. M O O N , MD Department of Cardiothoracic Surgery, Cleveland Clinic, Cleveland, Ohio

J E F F R E Y H. S I LV E R S T E I N , MD Department of Anesthesiology, Mount Sinai School of Medicine, New York, New York P E T E R S L I N G E R , MD, FRCPC Department of Anesthesia, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada C HA R L E S E. S M I T H , MD, FRCPC Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

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CONTRIBUTORS

PAU L S O E D I N G , MBBS, FANZCA Department of Anaesthesia and Pain Management, Department of Pharmacology, Royal Melbourne Hospital, University of Melbourne, Carlton, Victoria, Australia P. D AV I D Sø R A N , MD Department of Anesthesiology, Stanford University Medical Center, Stanford, California E L DA R Sø R E I D E , MD, P H D Department of Anesthesia and Intensive Care, University of Bergen, Stavanger University Hospital, Stavanger, Norway E L I Z A B E T H A. S T E E L E , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

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K U TA I B BA TA B BA A , MD Department of Anesthesiology, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio PAU L T E N E N B E I N , MD, FRCPC Department of Anesthesiology, Harborview Medical Center, University of Washington Medical Center, Seattle, Washington K A L PA NA T YAG A R A J , MD Department of Anesthesiology, Maimonides Medical Center, New York, New York H E AT H E R A. VA L L I E R , MD Department of Orthopedic Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio V E E R A BA D R A N V E L AY U T HA M , FRCA Department of Anesthesia and Perioperative Medicine, University of Western Ontario, London, Ontario, Canada

D E N N I S M. S U P E R , MD, MPH Department of Pediatrics, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

W I L L IA M C. W I L S O N , MD, MA Department of Anesthesiology, University of California San Diego Medical Center, University of California San Diego School of Medicine, La Jolla, California

A N N E J. S U TC L I F F E , MB, C H B, FRCA Department of Anesthesia and Critical Care, Alexandra Hospital, Worcestershire, United Kingdom

C HA R L E S J. YOW L E R , MD Department of Surgery, MetroHealth Medical Center, Case Western Reserve University School of Medicine, Cleveland, Ohio

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1 M E CHA N I S M S I N T R AU M A

AND

DEMOGRAPHICS

Pedro Barbieri, Daniel H. Gomez, Peter F. Mahoney, Pablo Pratesi, and Christopher M. Grande Objectives The aim of this chapter is to put trauma in context as a major health issue and give practitioners an understanding of the underlying causes and mechanisms.

INTRODUCTION Injury is the leading cause of death in people aged between 1 and 44 years in the United States and a leading cause of death worldwide [1]. It can be defined as a “physical harm or damage to the structure or function of the body, caused by an acute exchange of energy (mechanical, chemical, thermal, radioactive, or biological) that exceeds the body’s tolerance” [2, 3]. In 2002, 33 million patients were processed by emergency departments in the United States, and 161,269 died by traumatic injury [4]. Trauma is the leading cause of years of potential life lost for people younger than 75 years and this implies a huge expense to the health care system and massive amounts of resources used for care and rehabilitation [5]. Demographics is the statistical study of human populations, especially with reference to size and density, distribution, and vital statistics. Data on the demographics of trauma in the United States have been obtained from a number of sources listed in the references to this chapter. ALCOHOL In a recent report from the Federal Bureau of Investigation’s (FBI) Uniform Crime Reporting Program, the FBI estimated that more than 1.4 million drivers were arrested for driving under the influence of alcohol or narcotics, and an estimated 254,000 persons were injured in crashes where police reported that alcohol was present – an average of one person injured approximately every two minutes. In 2005, 21 percent of the children aged 14 and younger killed in motor vehicle crashes were killed in alcohol-related crashes.

Unintentional motor vehicle traffic-related injuries statistics: Between 2000 and 2004, 366,021 persons suffered injuries by unintentional motor vehicle-related injuries. Of these 266,491 were vehicle occupants, 37,340 were motorcyclists, and 43,502 were pedestrians [6]. In 2005, 43,200 victims died on the highways of the United States. Safety belts are approximately 50 percent effective for preventing fatality in severe crashes. Belts save 13,000 lives each year, while 7,000 persons die because they do not use belts. Air bags, combined with lap/shoulder safety belts, offer the most effective safety protection available today for passenger vehicle occupants. But, air bags are only to be regarded as supplemental protection to seat belts and are not designed to deploy in all crashes. Most airbags are designed to inflate in a moderate-to-severe frontal crash. In 2005, an estimated 2,741 lives were saved by air bags. Children from 0 to 14 years are at great risk for unintentional motor vehicle-related injuries. In 2004, 1,638 children died as occupants in motor vehicle crashes (5 deaths and 586 injuries each day) and half of those killed in motor vehicle accidents were unrestrained [7]. Twenty-five percent of occupant deaths among children younger than 14 years involve a drinking driver. Restraint use among young children depends on the driver’s restraint use; almost 40 percent of children riding with unbelted drivers were themselves unrestrained.

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Figure 1.1. Road traffic collision overview. Important prehospital information about the collision will be lost if hospital personnel do not get a good handover from prehospital crews. Photo courtsey of PF Mahoney.

UNINTENTIONAL MOTOR VEHICLE T R A F F I C - R E L AT E D I N J U RY M E C H A N I S M S Unless anesthesia providers are involved in prehospital care, their usual experience with trauma patients will be having them presented in the resuscitation room, packaged by prehospital ambulance crews (Figure 1.1). To understand what has happened to the patient and to appreciate the likely injuries, it is vital to get a clear handover. Information needed includes: ■ ■ ■ ■ ■ ■ ■

Estimated speed of vehicles involved Direction of impact Whether the vehicle rolled over Whether the occupants were wearing seat belts Whether the air bags deployed What damage occurred to the passenger compartment How long the extrication took.

To understand the magnitude of the injury, it is necessary to be able to develop a mental image of the interaction between energy and body anatomy, an intuitive concept and understanding about forces of acceleration–deceleration, and energy transferred to the body. Unintentional motor vehicle-related injuries involve a complex interaction of forces, including: ■ ■

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Primary collision: impact of vehicle with another object Secondary collision: the casualty strikes internal parts of the vehicle that may have intruded into the passenger compartment due to the primary collision Damage due to organs and tissue moving within the body and tearing vessels and attachments.

Unintentional motor vehicle-related injuries usually are categorized as: ■ ■ ■

Head-on or frontal Rear impact Side impact

Figure 1.2. High-energy impact on a car after casualty has been removed. Note the intrusion of metal into the occupant compartment. Significant injury can be expected. Photo courtsey of PF Mahoney.

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Rotational impact Rollover.

Examples of these injury mechanisms are shown in Figures 1.2–1.5. Half of deaths are related to head-on impact, and the rest involve side impact (25%), rear impact (less than 10%), and rollover [8]. An unrestrained front seat occupant is likely to suffer one of two injury patterns in a frontal impact, depending on whether the mechanism was “down and under” or “up and over.” With the down-and-under approach the passenger slumps in the seat and the knees move forward, usually striking the underside of the dashboard. Forces are transmitted through the femurs to the hips and pelvis, resulting in fracture-dislocation of hips. Impact of the feet on the floor causes fracture-dislocations and soft tissue damage below the knees. As the upper body moves forward, it hits the steering wheel, dashboard, and windshield, resulting in injury to the face, head, neck, chest, and abdomen. In the up-and-over pattern the face and head are the first points to strike the windshield, followed by the chest. Face and head injuries result, and cervical spine injuries occur as a result of extension and/or compression. Direct injury to the front of the neck from contact with the steering wheel, dashboard, or windshield may produce severe tracheal injuries [9]. Rear impact is frequently associated with whiplash injury. Depending on the forces involved and the amount and design of

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Figure 1.3. High-energy impact removing side structures of a vehicle. Significant injuries would be expected to vehicle occupants. Photo courtsey of PF Mahoney.

head restraint, injury may range from minor soft tissue injuries to extensive fractures with spinal cord injury. In the side collision, parts of the vehicle frame intrude on the passenger compartment. Because the side of the driver’s or passenger’s body is relatively exposed and unrestrained, injury may affect any region as the body strikes the side of the vehicle. The cervical spinal column is not tolerant of lateral forces, so cervical injuries are common in side impacts [10]. Complex patterns of injury arise from vehicle rollovers. The vehicle is often severely damaged, and the risk of ejection of unrestrained passengers is usually more significant than with other types of collision. The correct and incorrect use of seat belts may also produce specific patterns of injury. Lap belts offer little protection to the head and upper body and may cause lumbar spine and intraabdominal injuries to the duodenum, pancreas, small bowel, spleen, liver, and gravid uterus. A diagonal shoulder belt without a lap component allows the body to slide under, possi-

Figure 1.5. Building hit by a bus. Injuries to be expected include crush from falling bricks. Photo courtsey of PF Mahoney.

bly producing severe head and neck injuries. Wearing the diagonal component below the arm instead of above it may result in severe chest and abdominal injuries. Incorrect placement of the lap belt above the pelvis leaves the lower abdomen and lumbar spine susceptible to injury. Even the correct use of well-designed seat belts may result in injuries, the most common of which are fractures to the ribs, clavicle, and sternum [11].

M O T O R C YC L E C O L L I S I O N S TAT I S T I C S

Figure 1.4. Vehicle rollover can be associated with complex patterns of injury. Photo courtsey of PF Mahoney.

In 2005, in the United States, 4,553 motorcyclists died in motorcycle collisions and an additional 87,000 were injured. Comparing the vehicle miles traveled in 2004, motorcyclists were about thirty-four times more likely than passenger car occupants to die in a motor vehicle traffic crash and eight times more likely to be injured. Helmets are estimated to be 37 percent effective in preventing fatal injuries to motorcyclists. This means that for every 100 motorcyclists killed in crashes while not wearing a helmet, 37 of them could have been saved had all 100 worn helmets. Reported

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helmet use rates for fatally injured motorcyclists in 2005 were 58 percent for operators and 50 percent for passengers.

the impact. Head-first impact can produce facial-cranial injury, lesions of neck, cervical spine, shoulders, and pelvis.

M O T O R C YC L E C O L L I S I O N M E C H A N I S M S

T R AU M AT I C B R A I N I N J U RY ( T B I )

Injury to motorcyclists results from impact with the ground, street furniture, or the colliding vehicle. Injury can be expected to all body regions. Injuries of particular note include:

Traumatic brain injuries contribute to a substantial number of deaths and cases of permanent disability annually. Of the 1.4 million who sustain a TBI each year in the United States 50,000 die, 235,000 are hospitalized, and 1.1 million are treated and released from an emergency department. Among children aged 0 to 14 years, TBI results in an estimated 2,685 deaths, 37,000 hospitalizations, and 435,000 emergency department visits annually [12]. The leading causes of TBI are falls (28%), motor vehicletraffic crashes (20%), struck by/against events (19%), and assaults (11%) [13].

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Closed head injury Facial trauma Cervical spine fractures Chest injuries including injuries typical of deceleration such as aortic disruption Abdomen – liver and spleen injury Extremities – long-bone fractures.

PEDESTRIAN VEHICLE COLLISION

F I R E A N D B U R N D E AT H S

In 2005, in the United States, about 4,881 pedestrians were killed in traffic crashes and 64,000 were injured. On average, a pedestrian is killed in a traffic crash every 108 minutes and injured in a traffic crash every 8 minutes. Seventy percent of the pedestrians killed in 2005 were males; and 16 percent were older than 70 years. Forty-three percent of the 388 young (under age 16) pedestrian fatalities occurred in crashes between 3 p.m. and 7 p.m. and nearly one-half (48%) of all pedestrian fatalities occurred on weekends. Adult pedestrian injury typically involves three impacts:

Deaths from fires and burns are the fifth most common cause of unintentional injury deaths in the United States [14]. The average extent of a burn injury admitted to a burn center is about 14 percent of total body surface area (1991–93) while burns of 60 percent total body surface area or more account for 4 percent of admissions. Most victims of fires die from smoke or toxic gases and not from burns [15]. Smoking is the leading cause of fire-related deaths, and cooking is the primary cause of residential fires [16]. Approximately half of home fire deaths occur in homes without smoke alarms [17].

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Impact with the lower limbs as the impacting vehicle brakes and decelerates, lowering the front of the vehicle Impact with the hood of the vehicle as the casualty is thrown forward, causing head and chest injuries Impact with the ground, commonly causing head injury.

Pedestrian child injury is less predictable, but a typical pattern of trauma is “knocked down and run over,” resulting in chest, femur, and head injuries and secondary trauma resulting from hitting the vehicle or ground.

FA L L S Falls exceeded motor vehicle accidents as the leading cause of nonfatal injuries treated in hospital emergency departments in the United States in 2004. Falls are the most frequent cause of injuries and hospital admissions in the elderly population aged 65 years and older. Falls in the elderly are frequently associated with a concurrent medical event, such as cerebrovascular accident or myocardial ischemia. Falls involve a sudden deceleration in the vertical plane. The magnitude of injury depends on height, transference and absorption of energy, and orientation of the victim. Falls of 8 to 10 meters (25–30 feet, three stories in a building) are fatal in 50 percent of victims. If the victim is standing, foot, heel, tibia, fibula, femur, pelvis, spine, and internal organs can suffer

FIRE COSTS In 2005 residential fires caused nearly $7 billion in property damage [18]. Fire and burn injuries cost about $7.5 billion each year [5]. Fatal fire and burn injuries cost $3 billion. Hospitalized fire and burn injuries total $1 billion.

FIREARM – GUNSHOT In 2003, 30,136 persons died from firearm injuries in the United States, accounting for 18.4 percent of all injury deaths. Males had an age-adjusted rate that was 6.8 times that for females, the black population had a rate that was 2.1 times that of the white population, and the non-Hispanic population had a rate that was 1.3 times that of the Hispanic population. In 2004, the number of deaths due to homicides was 16,611, of which firearms homicides caused 11,250 deaths [19]. Homicide is the leading cause of death for black males aged 15 to 24 years, and 75 percent of homicides were firearm related. School shootings are devastating events that raise many concerns about the safety of the young population. However, the vast majority of youth homicides occur outside school hours and property. Fewer than 1 percent of the total number of children and youth homicides (5–19 years of age) is related to school shootings.

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P E N E T R AT I N G T R AU M A M E C H A N I S M S Low-Energy Transfer Sharp Implements Knives: The main issue to appreciate when managing knife wounds is that tissue is elastic. The dimensions of the observed wound in a patient may not relate to the weapon used. A knife assailant may turn the blade in the target’s body, causing increased damage as structures are deliberately cut. Swords: Different swords are designed to be used in different ways. For example, a sharp Samurai sword is designed with a cutting edge and if used in this fashion will produce injury different from a sword designed for thrusting, or another type, the broad sword. Projectiles Arrows: In general, injuries from arrows can be considered as “low-energy transfer” wounds and the area of injury is closely related to the arrow trajectory. This is not to dismiss how damaging arrows from a powerful bow or bolts from a crossbow can be. Bullets: Modern firearm ammunition is a combination of a projectile (the bullet) and a case. The bullet is held in the front end of the case. The case contains propellant. When this is

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Figure 1.6. These three pictures show a bullet entry wound (a), the path through the liver (b), and the exit wound (c). The extent of the injury only becomes clear at surgery or at forensic examination. On first inspection it is often difficult to be confident about which is the entry and which is the exit wound. Photo courtsey of PF Mahoney.

initiated the bullet is propelled down the barrel of the weapon. Many weapons have grooves inside the barrel that cause the bullet to spin, giving a degree of stability in flight, although bullets may become unstable in flight and “tumble.” The wounding effect on tissue is a combination of: ■ ■

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The properties of the tissue. Elastic tissue is pushed away; nonelastic tissue may shatter. The energy of the projectile. Kinetic energy of the projectile equals half the mass of the bullet times velocity squared (1/2 M × V × V). The energy transferred by the projectile to the tissue. This varies according to how the bullet strikes: nose first or side first. A larger surface of the bullet striking usually means more energy given up. Whether or not the projectile breaks up in the tissue. The resulting fragments cause their own wounds. Vital structures hit (Figure 1.6, see also color plate after p. 294).

There is an arbitrary division between high-velocity (2,000–2,500 feet per second) and low-velocity bullets, but a better terminology is “high- and low-energy transfer wounds” depending on how much energy is dumped into the tissue,

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which in turn is influenced by the preceding factors. Projectiles moving at more than 1,000 feet per second are associated with a significant “temporary cavity” in tissue – that is, the kinetic energy given up to the tissues forces them away from the missile tract – and this can be many times the size of the permanent cavity left by the missile. This temporary cavity generally lasts only a few milliseconds. Dirt and clothing can be carried into the wound by the projectile and drawn in by the vacuum effects of the temporary cavity, leading to wound contamination. Types of Bullets

Quaternary: all other effects, including fires from the explosive components or from ignited fuel, toxic effects of fumes, and exacerbation of medical conditions. There is a question as to whether human tissue from homicide bombers or bombs in crowded places that ends up embedded in another victim should be classified as a separate wounding mechanism. Practically, casualties will often have complex combinations of these mechanisms. ■

Some broad examples are: ■ ■ ■

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Full metal jacket: metal casing around a lead core. A nonexpanding round that produces a deep wound. Jacketed hollow point: an exposed hollowed lead tip allows expansion of the round on impact. Less tissue penetration than full metal jacket but more energy transfer to tissue. Soft point: exposed lead tip allows rapid expansion. Altered ammunition: actions taken after ammunition has been manufactured to increase the wounds produced, for example, altering the shape or structure to increase tumble or fragmentation in the body. (Military use of altered and expanding ammunition was limited by the 1899 Hague Convention.)

A casualty in a military vehicle blown up by a bomb may be sheltered from the worst of the fragments but injured by the blast wave and fires within the vehicle. A soldier injured by a roadside bomb may escape the blast effect but suffer multiple penetrating injuries from fragments.

This can lead to conflicting requirements during surgery and anesthesia and will be considered further in the chapter on military and field anesthesia. S U M M A RY This chapter has provided an introduction to trauma mechanisms and the wider impacts of trauma on the population and the economy. Clinical issues will be expanded in the relevant chapters throughout the book.

Explosive Munition Injury The injury produced by a bullet is the result of a complex interaction between the bullet and tissue. Injury produced by an explosive device is also the result of complex interactions that can be broken down into a number of mechanisms. Explosives are categorized as high order or low order depending on how rapidly they change their state once initiated. Highorder explosives undergo almost instantaneous change from solid to gas, rapidly releasing energy, and are associated with sudden increases in pressure and a supersonic shock wave/shock front. Low-order explosives change less rapidly and are not associated with the overpressure wave. Blast injury has been classified as follows: Primary:

due to the actions of the blast or overpressure wave. This can completely disintegrate a casualty. The blast wave interacts with the body or component tissue, dumping energy into the tissue and producing stress waves that cause microvascular injury and shear waves that produce asynchronous tissue movement, which causes tearing. Secondary: due to fragments projected by the energy of the explosion. Fragments can be “natural” from the random fragmentation of the bomb’s components, or “preformed” from notched wire, metal balls, or squares packed into the bomb. These cause multiple penetrating injuries. Tertiary: due to the casualty being thrown/displaced by the explosion or injured due to structural collapse. This is generally “blunt” injury.

M U LT I P L E C H O I C E Q U E S T I O N S

1. Which of the following is correct? a. Trauma deaths occur equally in all age groups. b. Sporting accidents are the leading cause of death in people older than 75 years. c. Falls in the elderly are often associated with events such as transient ischemic attacks or myocardial ischemia. d. Alcohol use is not associated with traffic collisions. 2. With regard to motorcycle collisions, which of the following is correct? a. When compared mile for mile, motorcycles are a safer mode of transport than cars. b. In motorcycle crashes only the riders’ limbs suffer injury. c. It is safe to use narcotics and ride motorcycles. d. Wearing a helmet can significantly reduce death from head injury in motorcyclists. 3. Considering children injured in road collisions, which of the following is correct? a. Children are rarely injured in road accidents. b. Alcohol use by a driver is a significant cause of children being injured both as passengers and as pedestrians. c. Children do not need to wear seat belts. d. Children have more flexible bones than adults so are not as badly hurt if hit by a car.

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MECHANISMS

4. Concerning adult pedestrians hit by cars, which of the following is correct? a. Adult pedestrians typically suffer three impacts when hit by a car – hit in the lower limbs, impact with the vehicle hood, then a further impact with the road. b. Weekends are the safest time for pedestrians. c. Males and females are injured equally in pedestrian collisions. d. Vehicle speed has no influence on pedestrian injuries suffered.

6. Which of the following statements about firearm incidents is correct? a. Firearm deaths in the United States affect males and females equally. b. Firearm deaths in the United States affect all ethnic groups equally. c. Firearm deaths in the United States affect all age groups equally. d. Less than 1 percent of the total number of children and youth homicides (5 to 19 years of age) are related to school shootings. 7. Concerning penetrating trauma, which of the following is true? a. All bullets have the same kinetic energy. b. Expanding ammunition was endorsed by the 1899 Hague Convention. c. The properties of the tissue struck by a bullet influence the injury produced. d. The kinetic energy of a bullet is given by its height multiplied by its weight. 8. Regarding knife injuries, which of the following is true? a. You can guess the length of the knife used to cause a wound by looking at the wound. b. Knives used for stabbing and swords used for slashing always produce identical wounds. c. If a patient presents with a knife in situ, wait until the patient is in the operating room before the surgeon takes it out. d. Knives always do more damage to people than bullets. 9. Concerning explosive injury, which of the following is true? a. Low-energy explosives cause a huge shock wave.

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b. A casualty in a vehicle will always be protected from the heat of an explosion. c. The effects of fires in an explosion are termed primary blast injury. d. The effects of fragments in an explosion are termed secondary blast injury. 10. With regard to trauma mechanisms, which of the following is true? a. Injuries after falling from more than twenty feet are generally very minor. b. Traumatic brain injury rarely occurs in the United States. c. The average size of burns admitted to burn centers is about 80 percent. d. Dirt and clothing fragments carried into a bullet wound are sources of contamination.

5. Regarding death and injury caused by fires, which of the following is correct? a. Carbon monoxide and flames cause an equal number of fatalities. b. Smoking at home when under the influence of alcohol is safe. c. Fire and burn injuries cost the United States about $1 million every year. d. Approximately half of home fire deaths occur in homes without smoke alarms.

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1. 2. 3. 4.

c d b a

5. d 6. d 7. c

8. c 9. d 10. d

REFERENCES

1. World Health Organization. (http://www.who.int/en). 2. National Safety Council. Accidents facts. Chicago 1990. The Council, Itasca, IL. (http://www.nsc.org/lrs/statinfo/odds.htm). 3. Fingerhut LA, Warner M. Injury Chartbook. Heart, United States, 1996–97. Hyattsville, MD: National Center for Health Statistics, 1998. National Health Interview Survey (http://www. cdc.gov/nchs/nhis.htm). 4. Minino AM, Anderson RN, Fingerhut LA, Boudreault MA, Warner M: Death: Injuries, 2002. Centers for Disease Control and Prevention (CDC). National Vital Statistics Report, National Center for Health Statistics, CDC, Atlanta, GA, Volume 54, Number 10, 2006 (http://www.cdc.gov/nchs/nvss.htm). 5. Finkelstein EA, Corso PS, Miller TR, Associates. Incidence and Economic Burden of Injuries in the United States. New York: Oxford University Press, 2006. 6. American College of Surgeons (ACS). National Trauma Data Bank Report 2005, ed. Fildes J, chair. (http://www.ntdb.org) (last update: November 12, 2006). 7. NHTSA’s National Center for Statistics and Analysis (NCSA). http://www.nhtsa.dot.gov/people/ncsa (last update: November 12, 2006) 8. Olding-Smee W, Crockard A. The trauma problem. In OldingSmee W, Crockard A, ed. Trauma Care. London: Academic Press, 1981, pp 3–18. 9. Butler RM, Moster FH. The padded dash syndrome and blunt trauma to the larynx and trachea. Laryngoscope 1968;78:1172– 82. 10. McSwain NE. Mechanism of injuries in blunt trauma. In McSwain NE, Kerstein MD, ed. Evaluation and Management of Trauma. Norwalk, CT: Appleton-Century-Crofts, 1987, pp 1–24. 11. Parr MJA, Grande CM. Mechanisms of trauma. In: Grande CM, ed. Textbook of Trauma Anesthesia. St. Louis: Mosby, 1994, chapter 36, pp 325–41.

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12. Langlois JA, Rutland-Brown W, Thomas KE. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2004. 13. Thurman D, Alverson C, Dunn K, Guerrero J, Sniezek J. Traumatic brain injury in the United States: a public health perspective. J Head Trauma Rehabil 1999;14(6):602–15. 14. Centers for Disease Control and Prevention. Web-based Injury Statistics Query and Reporting System (WISQARS) [Online]. 2005. National Center for Injury Prevention and Control, Centers for Disease Control and Prevention (producer). Available from: www.cdc.gov/ncipc/wisqars. (cited August 21, 2006). 15. Hall JR. Burns, Toxic Gases, and Other Hazards Associated with Fires: Deaths and Injuries in Fire and Non-Fire Situations. Quincy, MA: National Fire Protection Association, Fire Analysis and Research Division, 2001. 16. Ahrens M. The U.S. Fire Problem Overview Report: Leading Causes and Other Patterns and Trends. Quincy, MA: National Fire Protection Association, 2003. 17. Ahrens M. U.S. Experience with Smoke Alarms and Other Fire Alarms. Quincy, MA: National Fire Protection Association, 2004.

18. Karter MJ. Fire Loss in the United States during 2005, Abridged Report. Quincy, MA: National Fire Protection Association, Fire Analysis and Research Division, 2006. 19. McCaig LF, Nawar EW. National Hospital Ambulatory Medical Care Survey: 2004 Emergency Department Summary, Table 13. National Health Care Survey. Advance Data from Vital and Health Statistics. Number 372. June 23, 2006. Available at: http://www.cdc.gov/nchs/nhcs.htm.

OTHER SOURCES USED:

Pan American Health Organization (PAHO). (Demography in USA. 2005. (http://www.paho.org/eng) (last update: November 12, 2006). Maryland Family Health Administration (http://www.fha.state. md.us). Burn Foundation. A survey of 28 burn centers contributing data to the American Burn Association burn patient registry (1991–93); data from the National Burn Information Exchange (1965–85.) (http://www.burnfoundation.org/).

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2 T R AU M A A I R WAY M A N A G E M E N T William C. Wilson Objectives 1. Review the major considerations and tools needed for trauma airway management. 2. Characterize the difficult airway in trauma. 3. Evaluate the American Society of Anesthesiologists’ difficult airway algorithm with regard to trauma. 4. Provide a plan for managing common trauma difficult airway scenarios.

INTRODUCTION Airway management disasters account for a large proportion of malpractice lawsuits in the American Society of Anesthesiologists’ (ASA) Closed Claims database [1]. Airway loss is a major cause of preventable prehospital death in trauma patients [2]. Trauma airway management is complicated because of associated pathology and suboptimal intubating conditions, and also because complete preintubation evaluation and planning is rarely possible. Furthermore, trauma patients are at increased risk for hypoxia, airway obstruction, hypoventilation, hypotension, and aspiration. A significant reduction in airway management claims has occurred over the past decade due to the introduction of the ASA difficult airway algorithm, which institutionalized the need for airway evaluation, awake intubation techniques, and the use of back-up rescue modalities such as laryngeal mask airway (LMA), esophageal-tracheal-combitube (Combitube), and transtracheal jet ventilation (TTJV) [1]. It is therefore logical that incorporation of the ASA difficult airway algorithm, with certain minor modifications, can likewise improve safety during trauma airway management. This review of airway management for trauma begins with a survey of the equipment and drugs that should be prepared ahead of time, defines and characterizes the “difficult airway,” and describes the principles of airway evaluation and management for the trauma patient under both elective and emergency conditions. Proper evaluation and prioritization of treatment are emphasized throughout this chapter, with awake intubation techniques recommended for difficult airway management in cooperative, stable trauma patients. Emergency airway adjuncts such as the LMA and Combitube may be required to rescue the cannot intubate–cannot ventilate situation. Specific tips

are provided regarding the successful techniques and pitfalls of fiberoptic bronchoscopy, and the fiberoptic bronchoscopy technique is emphasized where appropriate throughout this chapter. After providing a survey of the major considerations and tools useful in trauma airway management, the ASA difficult airway algorithm is formally reviewed along with the suggested modifications required for trauma situations. With this foundation, the management of five common trauma difficult airway scenarios are reviewed. Important trauma airway complications are then summarized. Finally, new concepts and techniques that are currently being developed to improve trauma airway management are described. E Q U I P M E N T A N D D RU G P R E PA R AT I O N Regardless of the urgency associated with any particular intubation event, several key drugs and airway management tools are universally required; these should be available (and guaranteed to be in working order) for the physician providing airway management for the trauma patient. Essential emergency airway equipment items are listed in Table 2.1 and include: (1) an oxygen (O2 ) source and various types of administration devices; (2) an assortment of oral and nasal airways, along with a bag-valvemask ventilation device capable of applying positive pressure ventilation (and able to deliver 100% O2 ); (3) intubation equipment (including laryngoscopes, styletted and pretested endotracheal tubes [ETTs]); (4) suction tubing and a tonsil tipped suction device; (5) a functioning intravenous (IV) catheter; (6) prelabeled syringes containing induction and resuscitation drugs including vasopressors and inotropes; (7) appropriate monitors and intubation detectors (as will be described shortly). All of the aforementioned equipment (except for the 9

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Table 2.1: Essential Emergency Airway Equipment Contained in Portable Storage Unit for Trauma Resuscitation Equipment Category

Specific Emergency Airway Device

Oxygen

Oxygen (O2 ) inflow tubing and O2 source.

Ventilation

Bag-valve-mask device (connect to O2 source). Soft nasal airway Rigid oral airway Transtracheal jet ventilation equipment Laryngeal mask airway Esophageal-tracheal Combitube

Intubation

Laryngoscope with new tested batteries #3 and #4 Macintosh blades with functioning light bulbs #2 and #3 Miller blades with functioning light bulbs Endotracheal tubes – various sizes styletted with balloon tested Tracheal tube guides (gum elastic bougie, semirigid stylets, ventilating tube changer, light wand) Flexible fiberoptic intubation equipment Retrograde intubation equipment Adhesive tape or umbilical tape for securing ETT

Suction

Yankauer, endotracheal suction

Monitor

PET CO2 , pulse oximeter, esophageal detector device

Drugs

IV induction and paralytic medication Topicalization drugs deVilbiss sprayer for application of topical drugs Resuscitation drugs (epinephrine, atropine, etc.)

Miscellaneous

Various syringes, needles, stopcocks, IV connector tubes

ETT, endotracheal tube; IV, intravenous.

O2 source) should fit into a portable storage unit (i.e., Code Bag) for trauma resuscitation. In austere environments, small tanks of O2 will also need to be transported to the site of emergency airway management. The importance of each of these essential airway management devices and drugs will be reviewed in this section. Oxygen: Critical During Trauma Airway Management Advanced Trauma Life Support® (ATLS®) begins with assessment and management of the airway and breathing, the top two priorities in the ABCDEs of the primary survey. As soon as a trauma patient is encountered in the field or in the trauma bay, O2 is immediately applied. Furthermore, O2 should be administered throughout the trauma assessment and treatment phase. Hypoxemia is a constant threat in trauma and critical illness due to disease processes that cause respiratory failure and those associated with injury. In addition, 100 percent O2 should be administered for three to five minutes immediately preceding airway management (i.e., preoxygenation) to increase the duration of adequate O2 saturation during the period of postinduction apnea. Treatment of Hypoxemia Clinically, the term hypoxia denotes decreased O2 tension at the tissue level. Hypoxemia is defined as decreased O2 tension

in the arterial blood (PaO2 ). In trauma scenarios, when tissue hypoxia occurs, hypoxemia is nearly always present. Hypoxemia has eight major causes. The first five etiologies are related to the atmosphere (low partial pressure of inspired O2 ) or the lungs (hypoventilation, ventilationperfusion mismatch, right-to-left transpulmonary shunt, and diffusion abnormalities). The next two causes of hypoxemia involve delivery of O2 to the tissues (i.e., low oxyhemoglobin or low cardiac output). The final cause of hypoxemia is termed “histocytic,” denoting a problem in O2 utilization at the tissue level, usually due to the poisoning of the mitochondrial electron transport chain, as seen with cyanide or carbon monoxide toxicity. Patients suffering from all of these eight causes of hypoxemia will benefit from the administration of 100 percent O2 . Preoxygenation: Maximizing Arterial Saturation during Apnea During trauma airway management, O2 is administered prior to intubation in a process called preoxygenation. Optimum preoxygenation requires that 100 percent O2 be delivered by a tight-fitting mask during spontaneous ventilation for three to five minutes prior to administering drugs that cause apnea. If the time does not allow for a full five minutes of preoxygenation, the patient should be instructed to take four to eight vital capacity breaths; this will increase O2 stores, though not to the same level as a full five minutes of preoxygenation. The

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monary shunting, and further decreased FRC (atelectasis, lobar collapse) (Figure 2.2). Ventilation and Intubation Equipment

Figure 2.1. FRC and relationship of oxygen reserve. This figure illustrates the factors that determine the time from apnea until desaturation including the functional residual capacity (FRC), the concentration of oxygen in ˙ 2 ) of the patient. this reservoir (FIO2 ), and the oxygen consumption (VO The spirometric trace on the left side of the figure depicts the relative volumes of the FRC, tidal volume (VT), residual volume (RV), and vital capacity (VC). The reservoir of oxygen in the lungs at end exhalation (FRC) in a normal 70-kg patient is approximately 2.5 L, and the resting ˙ 2 is approximately 250 cc per minute. If the patient is breathing 100 VO percent oxygen then there are theoretically ten minutes prior to desaturation. Whereas, if the patient is breathing room air (21% oxygen) there are only two minutes prior to desaturation. Furthermore, ICU patients are ˙ 2 , and increased shunting, typically sicker with lower FRCs, increased VO all of which can cause more rapid desaturation following apnea. (From Wilson WC. Emergency airway management of the ward. In Hannowell LA, Waldron RJ, ed. Airway management. Philadelphia, PA: LippincottRaven Publishers, 1996, pp 443–51; with permission).

goal of preoxygenation is the replacement of nitrogen with O2 (denitrogenation), thereby increasing the O2 stores in the lungs, arterial and mixed venous blood, as well as in the tissues. Consequently, the duration that apnea can be tolerated, without causing arterial O2 desaturation, is prolonged. Preoxygenation is an essential component of any intubation technique that might involve a period of apnea. Preoxygenation is especially important for a “rapid sequence intubation” (RSI). When a patient is rendered apneic, the patient has a finite period of time prior to the onset of arterial desaturation. This time period is directly related to the reservoir of oxygen in the lungs at end exhalation during normal tidal breathing (the functional residual capacity [FRC]), and inversely related to the oxygen consumption (approximately 250 mL/min in a 70-kg patient) (Figure 2.1). Preoxygenation with 100 percent O2 allows for up to ten minutes of oxygen reserve following apnea in a normal patient at rest with healthy lungs and a normal FRC (approximately 2.5 L). The same patient when breathing room air (21% O2 ) would theoretically have about one fifth the time (only two minutes) prior to arterial desaturation. Furthermore, trauma patients frequently have a decreased FRC due to numerous causes (e.g. pneumothorax, hemothorax, rib fractures, diaphragmatic hernia, abdominal injuries, and intraabdominal blood), and will desaturate earlier than normal patients following apnea. Patients in respiratory failure from pulmonary edema, pneumonia, or pulmonary contusion will desaturate even sooner due to increased O2 consumption, increased right-to-left transpul-

An assortment of face masks should be available; and an appropriately sized mask should be attached to the manual ventilation device. The mask should be pre-tested for integrity and ability to generate positive pressure without leaks and should be capable of delivering 100 percent O2 at high flow rates. In austere environments, where O2 supplies are intermittent, a self-inflating device such as an AMBU® bag is recommended. Rigid oral and soft nasal airways should be available in small, medium, and large sizes for the adult patient. If managing pediatric airways, a pediatric kit with appropriately sized equipment must also be available (see Chapter 24). Various sized, styletted ETTs, with pretested balloons, should be prepared as follows. An adult-sized ETT (size 7.0 or 8.0) should have a malleable stylet passed through its interior to a position just short (5–10 mm) of the tip. The malleable stylet allows the distal end of the ETT to be molded into a configuration that will most easily pass through the patient’s vocal cords. In addition, a styletted 6.0 ETT (or 5.0 ETT) should be prepared as a backup for patients who have small glottic openings and/or difficult airways (smaller ETTs pass more easily into the trachea through swollen or edematous glottic openings). The rigid direct laryngoscope, with several blades, is the central piece of intubation equipment. The laryngoscope handle should be clean, and all electrical connections must be free of corrosion or debris. The batteries should be fully charged, and one should verify that a bright beam of light is generated when the blade is attached and extended into the working position. At least two sizes of Miller (#2 and #3) and two sizes of Macintosh blades (#3 and #4) should be provided in the kit, as each has advantages in certain types of airway problems. All of the items listed in Table 2.1 are essential and constitute the minimum airway equipment that should be contained in the portable storage unit. Suction Trauma patients, like other patients in respiratory failure, can have thick, tenacious, or bloody secretions, or they may have regurgitated. To minimize the risk of aspiration and to maximize visualization of the laryngeal anatomy, suctioning of the airway is frequently required during a trauma intubation. The suction apparatus should provide a continuous vacuum of sufficient force to rapidly clear oropharyngeal secretions or vomitus. During initial airway management, a large tonsiltype suction tip (e.g., Yankauer®) is best suited for suction of debris out of the oropharynx. After tracheal intubation, long, soft endotracheal suction catheters are most capable of clearing tracheobronchial secretions and aspirated material from the airways. Alternatively, a fiberoptic bronchoscope (FOB) can be used, postintubation, to remove plugs and secretions from specific lung segments under direct vision. The FOB can also be used to diagnose existing airway pathology and to confirm ETT position. Small, portable, battery-powered FOB devices are now available.

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Figure 2.2. SaO2 versus time of apnea for various types of patients. Time to hemoglobin desaturation with initial Fi O2 = 0.87. The SaO2 versus time curves were produced by the computer apnea model. The mean times to recovery from 1 mg/kg IV succinylcholine are shown in the lower right-hand corner. (From Benumof JL. Critical hemoglobin desaturation will occur before return to an unparalyzed state following 1 mg/kg IV succinylcholine. Anesthesiology 1997;87:979–82; with permission.)

Functioning Intravenous Catheter The ability to administer fluids, cardiovascular support drugs, and other medications is obviously essential in urgent and emergent conditions. Thus, after applying O2 by mask, assessing the airway, and ensuring ventilation, an IV should be established prior to attempting any airway manipulation to support the circulation, whenever time allows. If confronted with a patient in full arrest, the trachea should be intubated first and IV access secured immediately after initiating cardiopulmonary resuscitation (CPR), performing cardioversion, or implementing a resuscitative thoracotomy. Note that all Advanced Cardiac Life Support® (ACLS®) protocol drugs can be administered via the ETT except for highconcentration ionic compounds such as calcium, bicarbonate, and magnesium. The intraosseous route can be used as well. If access cannot be obtained, a central venous catheter should be placed (see Chapter 4). Monitoring and ETT Confirmation Devices Pulse oximetry, blood pressure (BP), and continuous electrocardiogram (ECG) constitute the appropriate minimal noninvasive monitoring that should be applied prior to attempting tracheal intubation. A complete set of vital signs is obtained when time allows. Vital sign stability and adequate arterial oxygen saturation are the goals prior to, during, and after intuba-

tion of the trachea. Immediately following a putative endotracheal intubation, the partial pressure of CO2 at the end of the exhaled breath (PET CO2 ) should be monitored. A number of devices and techniques for measuring PET CO2 are available and can be used to confirm ETT position and subsequently to assess ongoing ventilation adequacy. In situations with low or no cardiac output, an esophageal detector device is used to confirm ETT position. Both of these items should be contained in the portable storage unit (Table 2.1). Vasopressors and Inotropes Vasopressors must be available for immediate use because hypotension is a frequent accompaniment of trauma and critical illness. In addition, the administration of anesthetic drugs and the use of positive pressure ventilation can exacerbate or initiate hypotension in hypovolemic patients. Furthermore, premorbid conditions in previously ill or elderly patients will further increase the likelihood of hypotension following intubation. Portable Storage Unit for Trauma Resuscitation Equipment Commercially available toolboxes or soft duffel bags can be used for portable storage units. In addition to the aforementioned items, the adjunct equipment needed for assistance in managing

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Figure 2.3. Degree of airway difficulty continuum for mask ventilation and direct vision laryngoscopy at intubation. This illustration provides a conceptual frame work for the definition of airway difficulty with mask ventilation (Top) and direct vision laryngoscopy (Bottom). The degree of difficulty ranges from 0 degrees of difficulty to the impossible or infinitely difficult airway. The amount of difficulty can vary in the same patient with different anesthesiologist using various techniques. The grade of laryngoscopic view refers to grades defined by Cormack and Lehane (Figure 2.4) (From Benumof JL. Management of the difficult airway. Anesthesiology 1991;75:1087–110; with permission.)

the “difficult trauma airway” should be available. Each portable storage unit should be customized to meet the specific needs and preferences of the practitioner as well as the health care facility, and it should be stored in the trauma bay or brought there by the airway expert [5].

D E F I N I T I O N O F T H E D I F F I C U LT A I RWAY Airway difficulty can occur during bag-mask ventilation or during endotracheal intubation. The two are not synonymous; indeed, some patients who are difficult to ventilate (e.g., edentulous, bearded, large jaw) may be quite easy to intubate. Others who are difficult to ventilate (e.g., obstructive sleep apnea patients, abnormal neck anatomy) may be both difficult to bagmask ventilate as well as intubate. The difficulty of maintaining gas exchange by using bag-mask ventilation can range from a zero degree of difficulty to infinite (Figure 2.3). Difficulty of intubation using direct laryngoscopy also proceeds along a similar continuum from easy to nearly impossible (Figure 2.3). Difficult intubation has been defined as requiring multiple attempts with multiple maneuvers including external laryngeal manipulation, multiple laryngoscope blades, and/or multiple endoscopists [6]. Most recently, the ASA difficult airway guidelines defined difficult laryngoscopy as the impossibility of visualizing any portion of the vocal cords after multiple attempts using a conventional laryngoscope [5]. Probably the best definition of difficult intubation for documentation from one clinician to another and for research pur-

poses involves the grading of the laryngoscopic views as defined by Cormack and Lahane [7]. In the Cormak and Lahane classification (Figure 2.4), Grade I denotes visualization of the entire laryngeal aperture; Grade IV is visualization of only soft palate; and Grades II and III are intermediate views [3]. Grade III or IV laryngoscopic views correlate well with difficult intubations in the vast majority of patients [8, 9]. However, there are some clinically relevant situations that provide exceptions to this rule. First, the skill and experience of the endoscopist in manipulating the laryngoscope, the ETT, and the patient’s anatomy must be taken into account. Second, a Grade III laryngoscopic view has been described differently by different investigators [8, 10]. Third, the blade attached to the laryngoscope will affect the

Figure 2.4. Four grades of laryngoscopic view. The grading of laryngoscopic view is based upon the anatomic features that are visualized during the performance of direct laryngoscopy. (From Cormack RS, Lehane J. Difficult tracheal intubation in obstetrics. Anaesthesia 1984;39:1105; with permission.)

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Table 2.2: Anatomic/Pathologic Predictors of Difficult Intubation/Ventilation Anatomy

Difficult Ventilation

Difficult Intubation

Neck

Bull neck Obesity History of OSA

Bull neck Obesity Decreased head extension or neck flexion

Tongue

Large tongue

Large tongue

Mandible

Thick beard

Receding mandible Decreased jaw movement

Teeth

Edentulousness

Buck teeth

Maxillofacial

Facial fractures Lacerations Facial plethora

Facial fractures Facial plethora

Oropharyngeal

Edema Hematoma Inflammation Foreign body Tumor

Edema Hematoma Inflammation Infection/ abscess

Glottis

Edema Vocal cord paralysis Tumor

Edema Vocal cord paralysis Tumor

Neck

Penetrating or blunt injury Subcutaneous emphysema

C-spine injury Neck mass/hematoma Subcutaneous emphysema Ankylosing spondylitis Rheumatoid arthritis

Pathology

OSA, obstructive sleep apnea.

laryngeal view and therefore the assigned grade. Fourth, the blade selection can solve or exacerbate certain problems. For example, a long floppy epiglottis may yield a high-grade view (III, IV) with a Macintosh blade and a relatively low-grade view (I, II) if a straight blade is used. Finally, traumatic conditions such as cervical spine (C-spine) injury (i.e., inability to move the neck into a “sniffing position”), laryngeal fractures, or expanding hematomas may disassociate the laryngoscopic view from the difficulty of tracheal intubation. Despite these considerations, the laryngoscopic grading of Cormack and Lehane is used by most authors to define intubation difficulty and should be documented for each patient intubated [7]. Historical Indicators of Airway Difficulty The intent of obtaining an airway history is to elicit previously known factors indicating that airway management has been difficult in the past. Any patient who is awake and capable of coherent conversation should be asked about prior intubation and ventilation successes or failures. Some patients possess a Medic Alert bracelet indicating a history of difficult intubation or ventilation and this can be useful in obtunded patients. Regardless of the patient’s mental state, if time permits, the physician should review the patient’s chart for details of previous intubations and other concurrent problems that may com-

plicate intubation. If an obese patient relays that s/he requires nasal continuous positive airway pressure at night to sleep, this may indicate that mask ventilation and/or intubation will be more difficult than in a thin patient without such history. Pathologic/Anatomic Predictors of Airway Difficulty In the trauma setting, numerous lesions (hematoma, foreign body, and facial fractures/edema) can pose difficulty for spontaneous ventilation as well as bag-mask ventilation and intubation (Table 2.2). Suspected C-spine injuries pose intubation difficulty due to inability to extend the head on the neck or flex the neck on the chest. Other trauma conditions that make intubation difficult include burns and other inflammatory conditions where massive edema can impair the laryngoscopic view. Similarly, stab wounds or blunt trauma to the soft tissue in the neck can cause expanding hematomas or airway disruption to occur. Anatomic predictors (Table 2.2) of difficult mask ventilation and subsequent intubation may be evident before formal examination. Morbid obesity poses difficulty with mask ventilation due to inadequate mask fit and difficulty with holding the mask to the massive face with only one hand. In addition, ventilatory efforts are less effective due to the decreased compliance of the chest wall. Obese patients are also problematic due to

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Table 2.3: Eleven-Step Airway Examination of Benumof ∗ Step

Airway Examination Component

Nonreassuring Findings

Can Evaluate in Trauma Patient

1

Length of upper incisors

Relatively long

YES

2

Maxillary–mandibular incisor relationship

Prominent “overbite”

YES

3

Ability to prognath jaw

Unable

YES

4

Interincisor distance

70

14

25–30

8.5

6.5

LMA MFGR

Size

Classic™ Classic™

Largest ETT Inside LMA (ID mm)

Largest FOB Inside ETT (mm)

Classic™ LMA (LMA North America, Inc. San Diego, CA.). Cookgas® ILA™ (Mercury Medical, Clearwater, FL.).

needle is confirmed to be intratracheal, a wire is passed through the needle into the trachea by using the Seldinger technique. Maintaining the guidewire several centimeters into the trachea, the cricothyrotomy site is dilated. Then, using the Seldinger technique, the cricothyrotomy tube is advanced, confirmed to be intratracheal and secured in place.

CRICOTHYROID OTOMY – OPEN

Cricothyroidotomy is the emergency surgical airway of choice (versus tracheostomy) because there is less bleeding and a decreased insertion time due to the ease of determining anatomic landmarks (Figure 2.25). The thyroid cartilage is stabilized and an incision is made through the skin and

Figure 2.20. Fastrach™ LMA. Intubating laryngeal mask airway (ILMA), illustrating the rigid curve and handle. Notice the different window compared with standard LMA. (Courtesy of LMA North America, Inc., San Diego, CA.)

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Figure 2.21. A patient can be continuously ventilated during fiberoptic intubation using the laryngeal mask airway (LMA) as a conduit for the fiberoptic bronchoscope (FOB). By passing a 4.0-mm-OD fiberscope through the self-sealing diaphragm of a bronchoscopy elbow adaptor and the tip of a cuffed 6.0-mm-ID endotracheal tube (ETT) to the level of the grille on the LMA, ventilation can occur around the FOB but within the lumen of the ETT; the deflated cuff of the ETT inside the shaft of the LMA makes a tight enough seal to permit positive pressure ventilation. Once the FOB is passed well into the trachea, the 6.0-mm-ID ETT is pushed over the FOB into the trachea until the adaptor of the ETT is against the adaptor of the LMA (From Benumof JL. Laryngeal mask airway and the ASA difficult airway algorithm. Anesthesiology 1996;84:686–99; with permission.)

subcutaneous tissue overlying the cricothyroid membrane. The membrane is then opened with a stab incision, an endotracheal tube or cricothyrotomy tube is inserted, and placement is confirmed in the usual fashion. Of note, whenever conditions and time allow for a formal tracheostomy, it is favored over the emergency cricothyroidotomy, because of the decreased risk of subglottic stenosis, which more frequently occurs with cricothyrotomy. T R AC H E O S T O M Y

Tracheostomy is less desirable in emergency airway scenarios than cricothryoidotomy because it is slower and has greater

Figure 2.23. This figure demonstrates a 14-gauge angiocatheter passing through the cricothyroid membrane at an angle approximately 30 degrees caudad from the skin. After achieving this position the metal stylet is withdrawn and a syringe is applied to the catheter to confirm intratracheal position; aspiration of air is the expected end point if the 14-gauge catheter is truly in the tracheal lumen. (From Benumof JL, et al. Transtracheal ventilation. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: Lippincott-Raven Publisher, 1992, p 199; with permission.)

Figure 2.22. Rigid bronchoscope with ventilating side port and optic guide. Several sizes are shown.

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and potentially the thyroid isthmus. Once the first few tracheal rings are exposed, a horizontal incision is made between the first and second tracheal rings and the tube is introduced into the trachea. Percutaneous placement of a tracheostomy tube can be performed but is recommended under bronchoscopic guidance to reduce the chance of paratracheal insertion and to document real-time intratracheal position of the needle, wire, dilators, and the tracheostomy tube.

7

6 11

4

8

Blind Intubation Techniques: Not Recommended with Stridor

10

5

9

3

1 2

Figure 2.24. This figure demonstrates the equipment used for pressurizing the already placed transtracheal catheter. (1) Wall oxygen pressure quick disconnect device. (2) Green Chemtron O2 hose. (3) NPT hose barb connector. (4) Bird regulator gauge (0–50 psi). (5) NPT air hose connector. (6) High-pressure, self-coiling air hose. (7) Jet injector valve. (8) NPT hose barb connecting the injector valve to clear soft flexible tubing (9). (10) Hose barb connecting to the clear tubing with a standard Becton/Dickinson male Luer lock connector. (11) Transtracheal ventilation IV catheter with standard hub. (From Benumof JL, Scheller MS. The importance of transtracheal jet ventilation in the management of the difficult airway. Anesthesiology 1989;71:769–78; with permission.)

potential for bleeding. Optimally, a transverse skin incision is made in midline position for cosmetic and healing purposes. However, in emergency situations with novice surgeons, a vertical incision can be made in the midline of the neck to minimize bleeding and to avoid the anterior jugular veins overlying the trachea (Figure 2.26). Next, skin and subcutaneous tissue are divided with a scalpel through the platysma, the strap muscles,

Blind intubation techniques are contraindicated in the setting of stridor, known mass expanding lesions, or known partial airway injuries where blind manipulation can change a partial airway obstruction into a complete obstruction. Blind Nasal Intubation Blind nasal intubation is contraindicated in the presence of maxillofacial trauma where fracture of the cribriform bone is possible and in the setting of nasal bleeding or coagulopathy. When performing a blind nasal intubation, the patient should be sitting upright at 45 degrees (rarely appropriate in the acute trauma setting), spontaneously ventilating, and, optimally, awake and cooperative. The ETT is placed in the already dilated and anesthetized nasal passage and the airway expert’s ear is placed near the 15-mm connector end of the endotracheal tube. As the ETT is passed down the nasal passage toward the glottic aperture, the airway sounds from the patient will become louder. When the airway sounds are loudest, the patient should be instructed to pant or take some deep breaths, which then opens the glottic aperture, at which point the ETT should be advanced during inspiration. Using this maneuver, the ETT is most likely to enter the larynx due to the patient’s inhalation efforts. It is occasionally beneficial to use a special flexible tipped ETT known as an endotrol™ tube during blind intubation

Figure 2.25. Surgical cricothyroidotomy. Horizontal skin incision, incision of cricothyroid membrane, dilation of the opening, and introduction of a ventilation tube (From Biro P, et al. Transtracheal access and oxygenation techniques. Acta Anesth Scand 1998;42:169; with permission.)

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Figure 2.26. Tracheostomy. (A) Transverse incision made usually for elective tracheostomy but a vertical incision allows for less bleeding when emergent procedure done. (B) The strap muscles are separated and (C, D) thyroid isthmus retracted caudally. (E) After the second tracheal ring is cleaned off, an inferiorly based flap is developed in the tracheal wall and sutured to the skin to allow easy access to the trachea while the tract matures. (From “Head and Neck” In Greenfield LJ, et al., ed. Surgery: Scientific Principles and Practices. Philadelphia, PA: Lippincott-Raven Publishers, 1997, p 644; with permission.)

attempts. The endotrol™ tube allows the operator to flex the ETT anteriorly while advancing the tube (Figure 2.27). Clinical end points alerting the physician that the ETT has entered the patient’s trachea include: (1) the patient is no longer able to speak, (2) increased secretions are heard emanating from the ETT with exhalation, and (3) coughing is elicited as the ETT passes down the larynx into the trachea. Because clinical end points are imprecise, the endotracheal position must be confirmed just as with any other method of intubation using PET CO2 , and so on. Light Wand Although the light wand is often used electively in anesthetized patients, it can be used as an adjunct in the cannot intubate–cannot ventilate patient. All commercially available

light wands consist of a lighted stylet over which an ETT fits. The patient is anesthetized and the ETT with lighted stylet is passed into the oropharynx. Pulling the tongue out can frequently facilitate passing the light wand into the trachea. Once the ETT passes through the cords and enters into the larynx it produces a “jack-o’-lantern” effect due to transillumination of light (Figure 2.28). The transillumination is very prominent when the room lights are dimmed but may be difficult to appreciate in bright-light settings. Once the light wand is in the larynx, the ETT is advanced and the stylet is withdrawn. Confirmation that the ETT is in proper tracheal position must then be accomplished using PET CO2 and other standard means. The light wand technique is widely applicable to many situations and environments. It has been used successfully in patients when conventional laryngoscopy may be difficult such as small mouth opening, large protruding teeth, and decreased head

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Figure 2.27. Flexible tipped (Endtrol®) nasotracheal tube. The flexible tipped nasotracheal tube can greatly aid blind nasal tracheal intubation. By pulling the ring, the endotracheal tube (ETT) flexes more anterior, this helps direct the tip around the soft palate and into the laryngeal inlet. (See inset.) (From Ward CF, Salvatierra CA. Special intubation techniques for the adult patient. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: J. B. Lippincott Co., 1992, p 154; with permission.)

Figure 2.28. Transillumination of the larynx with light wand. This diagram demonstrates the jack-o’-lantern effect caused by transillumination of the soft tissues on the neck when the light wand enters the larynx. The left panel demonstrates the position of the light wand on entry into the laryngeal inlet. The middle panel demonstrates this view from the anterior orientation and the right panel shows a side view of the light wand in position to cause transillumination of the anterior structures. (From Ward CF, Salvatierra CA. Special intubation techniques for the adult patient. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: J. B. Lippincott Co., 1992, p 175; with permission.)

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Table 2.6: Regional Anesthesia and the Trauma-Related Difficult Airway Consideration

Regional Might Be Indicated

Regional Contraindicated

Injury location

Superficial, extremity

Head, chest, abdomen

Mental status

Sober, cooperative, minimal sedation needed

Altered sensorium, decreased mental status

Urgency

Can stop surgery at any time

Unsafe to interrupt surgery to establish a definitive airway.

Airway access

Good access to airway

Poor access to airway

Tolerate awake intubation if necessary

Agreed to awake intubation if necessary

Failure to agree on awake intubation if necessary

Hemodynamic status

Hemodynamically stable

Hemodynamically unstable

extension [14a, 14b]. The light wand is contraindicated in the presence of stridor or obvious airway trauma (as are all “blind” intubation techniques).

Glidescope The Glidescope consists of a digital video camera embedded within a modified laryngoscope blade [14c]. The blade is similar to a Macintosh but has a pronounced 60 degree angulation. An LED light source mounted beside the camera provides continuous illumination. The glottic structures and intubation sequence are displayed on the video monitor. The Glidescope usually provides a grade 1 view of the larynx following which the tracheal tube is advanced toward and through the glottic opening. Successful intubation is facilitated by use of a stylet within the advancing ETT, or with a gum-elastic bougie. The video camera is equipped with an antifogging device. In a large multicenter trial of 728 patients, Glidescope laryngoscopy consistently yielded excellent or good laryngeal exposure [14d]. Successful intubation was generally achieved with the Glidescope even when conventional laryngoscopy was predicted to be difficult.

Retrograde Wire Less commonly performed due to its time requirement, the retrograde technique was first described by Ralph Waters in 1963 where he employed a Tuohy needle to pass through the cricothyroid membrane in a cephalad direction [28]. An epidural catheter was then threaded through the Tuohy needle and the catheter was retrieved from the oropharynx by using a plastic dressmaker’s hook. Next, both the tube and the catheter were withdrawn from the nares. In 1967, Powell and Ozdil introduced a wire-through-the-needle technique and in their modification, the wire was placed through the Murphy side hole of the ETT [29]. Placing the wire through the Murphy side hole allowed for the ETT to pass further through the cords than when the wire went out the tip of the ETT. Other modifications of these techniques have been described but the basic technique remains the same. Indeed, the Cookgas® Critical Care division has developed an emergency retrograde intubation kit (Cookgas® Mercury Medical, Clearwater, FL).

Regional Anesthesia in the Trauma Patient with Known Difficult Airway Occasionally, anesthesia can be achieved without securing the airway of a patient with a known difficult airway. In the cooperative and hemodynamically stable trauma patient with a solitary superficial extremity injury, a regional technique can be utilized so long as the patient understands and agrees to a plan that an awake intubation may need to be done if conditions change and warrant it (Table 2.6). In the patient with head or torso trauma, or an altered sensorium, a regional anesthetic is unwise because airway access is compromised, making a controlled awake intubation impossible. F I B E R O P T I C B R O N C H O S C O P Y: T E C H N I Q U E S A N D P I T FA L L S A FOB-assisted intubation is optimally performed in awake patients who are breathing spontaneously, but can also be used in anesthetized or apneic patients. There are many recipes for accomplishment of FOB-guided intubation. Success with FOB-guided intubation requires appropriate patient selection and preparation along with appropriate technique and adequate experience because conditions can vary in different patients, requiring the skill of the endoscopist to achieve success (Table 2.7). Patient Selection Indications for FOB intubation include: (1) situations where alignment of the oral pharyngeal and laryngeal axes is difficult or ill advised (i.e., C-spine injury or neck fixed in halo, (2) situations where direct laryngoscopy is expected to be difficult [i.e., hyomental distance (HMD)] less than 6 cm, Mallampati Class III or IV (Figure 2.5), especially situations with small mouth openings and in temporomandibular disease. Contraindications to FOB intubation include massive oropharyngeal hemorrhage (unable to adequately see) and conditions where time for adequate topicalization does not exist, such as profound hemodynamic instability or life-threatening airway obstruction. Relative contraindications for FOB intubation include copious secretions or friable tissues that are difficult to manage with antisialagogues and careful manipulation of the FOB.

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Table 2.7: Causes of Failure to Intubate with Fiberoptic Bronchoscope Cause of Failure

Comments and Solutions

Patient selection factors Massive bleeding

These constitute relative contraindications to FOB Unable to visualize airway. Small amounts of bleeding can be controlled with frequent suctioning. A vasoconstrictor added to topical agents helps limits bleeding. Patient will not hold still and or is very belligerent. Rare in elective situations, but common in trauma and emergency scenarios. Does not allow time to properly topicalize airway

Uncooperative patient Patient too unstable Patient preparation factors Inadequate topical anesthesia

Presence of secretions or small amounts of blood Patient desaturates during FOB Endoscopist experience factors Inability to navigate normal anatomy Distorted anatomy due to tumors or abscess Inability to visualize cords due to a large floppy epiglottis Fogging of objective Inability to advance tube into trachea

Inability to remove the FOB

Be patient, take time to topicalize properly. Dry mucosa (glycopyrrolate), suction secretions from the oropharynx so that topical anesthesia can reach mucosa to work. Anesthetize the nose, nasopharynx, oropharynx, larynx, and trachea. Nerve blocks usually unnecessary with proper topicalization. Treat with proper suctioning, use of an antisialagogue (glycopyrrolate) and a vasoconstricting agent (neosynephrine) or use cocaine. Attach O2 to suction port of FOB, blowing secretions away. Patient should be wearing nasal prongs or mask O2 during FOB Also, endoscopist can attach O2 to the suction channel of the FOB and instruct patient to pant during intubation. Most common problem of novice is too little practice with airway models and mannequins prior to attempting to intubate patients. Excellent indications that use of a FOB as intubation with direct laryngoscopy may be difficult. However, the endoscopist must be well grounded in normal anatomy prior to managing difficult airways. Have patient say “Ahh” and or pant “like a puppy.” (If patient is anesthetized, assistant can apply jaw thrust or pull the tongue out) Use a dilute detergent (Chlorhexidine) to wipe the FOB lenses prior to use, warm the FOB prior to use. Inadequate topical anesthesia – perform nerve block or use more topical. Large discrepancy between ETT and FOB – use the largest FOB that will fit easily thru the ETT yet still allow easy removal with proper lubrication. Hung up at glottic opening. Pull back the ETT and rotate 90◦ to 180◦ either right or left to allow the ETT to pass thru the cords more easily. Beware the FOB may exit the Murphy eye of the ETT. This can be avoided if the FOB is threaded through the ETT prior to attempting intubation. Some endoscopists will place the lubricated ETT through the nares into the nasopharynx blindly and then pass the FOB through the ETT. This technique has greater risk of FOB exiting the Murphy eye. Also, be sure that the FOB is well lubricated with silicone or Xeroform gauze prior to placing thru the ETT.

FOB, fiberoptic bronchoscope; O2 , oxygen; ETT, endotracheal tube.

Oropharyngeal tumors, abscesses, maxillofacial trauma, and most causes of stridor are optimally managed with awake techniques, and should all be considered as good indications for FOB-assisted intubation, providing the endoscopist can avoid blood and see the entire way into the trachea. Patient Preparation Positioning for FOB Optimally, the patient is placed into a sitting position; in patients with C-spine injuries, this can be allowed as long as there is no thoracolumbar spine injury. Nasal cannula oxygen is administered, and pulse oximetry and other monitoring devices are applied. The sitting position allows secretions to run down into the esophagus and out of the bronchoscopic view. Gravity also helps direct the fiberoptic bronchoscope toward the larynx as compared with the supine position, where gravity tends to favor the posterior esophageal orifice.

Analgesia, Sedation, and Antisialagogue Patients should receive an antisialagogue (glycopyrrolate, 0.2 mg) and sedation prior to starting the procedure. Opioids, benzodiazepines, dexmedetomidine, and droperidol have all been used successfully. However, low-dose opioids alone (fentanyl, 1–2 μg/kg) are usually sufficient in patients who are not opioid-tolerant. Midazolam can cause some patients to become hyperalgesic and uncooperative; yet, many have used this (and other) benzodiazepines successfully. Fentanyl is often adequate as a sole agent because it provides sedation as well as analgesia, both of which are useful while topicalization is occurring. Dexmedetomidine infusion provides excellent sedation, decreases opioid requirements, attenuates tachycardia, and minimally depresses ventilation. Local Anesthesia and Vasoconstriction The described technique of mucosal topicalization and vasoconstriction can be used for FOB-guided ETT placement

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as well as with other awake airway devices. The patient should receive phenylephrine or oxymetolazone nasal spray applied into both nares prior to initiating topicalization. Next, the patient should be asked to report which nares allows for better airflow. This will identify the nares that should be intubated and primarily topicalized. However, both nares should be topicalized to block both the right and left superior laryngeal nerves and more fully anesthetize the supralaryngeal structures. The nasopharynx, oropharynx, base of the tongue, and larynx should all be anesthetized. The nasopharynx can be anesthetized with either 4 percent cocaine or 4 percent lidocaine mixed with dilute phenylephrine. For nasopharyngeal anesthesia, 4 percent cocaine, although slightly more toxic, can be more efficacious, because of its inherent intense vasoconstriction coupled with a more rapid onset and a longer duration of action than lidocaine. The toxic dose of cocaine is 3 mg/kg, whereas the toxic dose with lidocaine is 7 mg/kg when used with vasoconstriction. Cocaine is topically applied to each nare by using Krause’s forceps (Figure 2.29) or a cotton-tipped applicator (Q-tip®). Topicalization is initiated by painting the external nares and slowly working down the nasopharynx with the cocaineimpregnated Q-tip®. By advancing the Q-tip® into the pyriform fossa, the superior laryngeal nerve will also become blocked. The superior laryngeal nerve innervates the epiglottis, aryepiglottic folds, and mucus membranes of the laryngeal structures down to the false cords. When the Q-tip® can be inserted into the deepest recesses of the nasal cavity without causing discomfort, a soft 34 French nasal airway can be inserted. If the patient is not

Tongue Epiglottis

Pyriform recess

Superior laryngeal nerve Krause's forceps Gauze with local anesthetic Pyriform recess Internal barnch of superior laryngeal nerve

Figure 2.29. Superior laryngeal nerve block by external approach (“topicalization”). Posterior view of the nasopharyngeal area showing the perforating branches of the superior laryngeal nerve. Krause’s forceps are used with gauze soaked in local anesthetic fluid at the level of the pyriform sinus. (From University of California, Irvine, Department of Anesthesia D.A. teaching aids; with permission.)

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Figure 2.30. Continuous oxygen flow atomizer apparatus. Oxygen tubing is connected from an oxygen tank to the bulb attachment site of a DeVilbiss atomizer. A hole is cut in the oxygen tubing near the attachment site. Oxygen is allowed to flow into the tubing and out of the cut hole until a finger is applied covering the hole; then oxygen flows to the nebulizer and a fine mist of local anesthesia is emitted. The size and velocity of the spray is directly related to the flow of oxygen through the tubing. (Reproduced with permission from Benumof JL. Anesthesia for Thoracic Surgery, Philadelphia, PA: W. B. Saunders, 1987, pp 241–3; with permission.)

inconvenienced by this, the topicalization of the nasopharynx is complete. While the nasopharynx is being anesthetized, simultaneous topicalization of the oropharynx and larynx should occur by spraying a fine mist of 4 percent lidocaine via a DeVilbiss nebulizer. The DeVilbiss sprayer can be modified by connecting it to a low-flow O2 source after removing the squeeze bulb, thus providing a continuous source of aerosolized lidocaine (Figure 2.30). When utilizing the DeVilbiss sprayer in this way, the patient can entrain the aerosolized lidocaine well into the trachea and past the carina. The patient should be instructed to “pant like a puppy dog” to facilitate the inhalation early in the process. Later, the patient will be able to inhale a full vital capacity breath of the aerosolized local anesthetic, indicating the subglottic structures are anesthetized. Once the DeVilbiss sprayer can fully enter the oropharynx without the patient gagging, oropharyngeal and base of tongue topicalization is adequate for fiberoptic intubation. Provided the patient has breathed enough lidocaine mist into the airways, the trachea is usually adequately anesthetized at this point as well. Some endoscopists prefer performing nerve blocks of the glossopharyngeal nerve at the palatoglossal arch (Figure 2.31) and the superior laryngeal nerve externally, where it crosses the superior cornu of the hyoid (Figure 2.32), as well as administering transtracheal lidocaine (Figure 2.33) [30]. These maneuvers are not necessary for FOB-aided or blind nasal intubation techniques in properly topicalized patients. However, if awake laryngoscopy is planned with either a conventional laryngoscope, or other device utilizing a blade (e.g., Bullard laryngoscope, Wu Scope, or Airtraq), the deep mucosal pressure receptors require blockade to prevent gagging. When these pressure-inducing rigid laryngoscopic devices are used to intubate awake patients, supplemental glossopharyngeal nerve blocks should also be performed (see Figure 2.33 legend for instructions). Technique of Fiberoptic Intubation Awake Nasal Technique The largest ETT that will fit the patient’s nasal passage should be used and most adults can accept an 8.0 ETT. Indeed,

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A Cornu of hyoid cartilage

Figure 2.31. Glossopharyngeal nerve (lingual branch) block. The tongue is pushed medially with a tongue depressor, and a three-inch spinal needle is inserted into the base of the anterior tonsillar pillar 0.5 cm lateral to the base of the tongue and advanced 0.5 cm deep. After negative aspiration, 2 mL of local anesthetic is injected. Both sides are injected for adequate block of the gag reflex. (From Mulroy MF. Regional Anesthesia: An Illustrated Procedure Guide, 3rd edition. Philadelphia, PA: Lippincott Williams and Wilkins, 2002, p 229; with permission.).

provided the patient’s nares can be easily dilated with a 34 French soft nasal airway, an 8.0 ETT will almost always fit through the nares. This is possible because the external diameter of a 34 French soft nasal airway is approximately 11.0 mm, whereas the external diameter of an 8.0 ETT is approximately 10.5 mm. However, in emergency situations, and in cases of stridor, smaller ETTs are best. Following topicalization, the FOB (Figure 2.34), with preloaded ETT, is inserted into the patient’s nares. Alternatively, an ETT can be placed in the nares to serve as an introducer and the FOB can then be placed through the ETT and into the nasal passage. The advantage of preloading the ETT over the FOB is elimination of the possibility that the FOB might exit the Murphy eye during intubation, which subsequently will not allow the ETT to enter the trachea. The advantage of the second technique is that the ETT serves as a dilating airway and a guide for the FOB. When the FOB exits the nasopharyngeal located ETT, it is frequently aiming directly into the laryngeal aperture. When manipulating the FOB, it is useful to remember that small movements at the end of the FOB result in very large changes in the view that the endoscopist has. Regardless of the technique chosen for introducing the FOB into the nares, the endoscopist next advances the FOB under direct vision until the epiglottis or the laryngeal aperture is visualized (Figure 2.35). The FOB should never be advanced blindly, because structures that are not clearly identified can be damaged. Once

Superior laryngeal nerve

Superior cornu of thyroid cartilage

Thyroid cartilage

B

Figure 2.32. Superior laryngeal nerve block. The 23- or 25-gauge needle is introduced onto the superior border of the lateral wing of the thyroid cartilage or caudad to the greater cornu of the hyoid bone. After negative aspiration deep to the thyrohyoid membrane, 2–3 mL of local anesthetic are injected into the space below the membrane. (From Norton ML. Atlas of the Difficult Airway: Topical and Regional Anesthesia of the Upper Airway. St. Louis, MO: Mosby Publishing, 2002, p 91; with permission.)

the glottis or the epiglottis is in view, the FOB is maneuvered through the vocal cords and into the trachea. The FOB is then advanced further down the trachea to a position just above the carina (Figure 2.35C). At this point, the ETT is threaded over the indwelling FOB, through the larynx and into trachea. If the ETT does not advance easily, it may be hung up at the arytenoids or at the laryngeal aperture. This can result from a large discrepancy between the internal diameter of the ETT and

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Fiberoptic bronchoscope ET tube threaded over fiberoptic bronchoscope insertion tube

Eye-piece

Flexible tip of insertion tube Insertion tube

Figure 2.33. Transtracheal injection (topical subglottic anesthesia – recurrent laryngeal nerve distribution). A 20-gauge IV catheter is introduced through the cricoid membrane. Once tracheal entry is confirmed by air aspiration, 4 mL of topical anesthetic is injected as the patient inspires; the inward airflow carries the solution down the trachea, and the cough reflex will spread it up to the undersurface of the vocal cords. (From Mulroy MF. Regional Anesthesia: An Illustrated Procedure Guide, 3rd edition. Philadelphia, PA: Lippincott Williams and Wilkins, 2002, p 230; with permission.)

the outer diameter of the FOB, or because the ETT is simply too large for the glottis. Often rotating the ETT 90–180 degrees either clockwise or counterclockwise will facilitate passage of the ETT through the glottic aperture. If the ETT will not pass despite the use of these maneuvers, then the ETT and FOB should be removed together as a unit and a smaller ETT utilized. If secretions become a problem during bronchoscopy, these can be managed by flushing saline down the working channel of the FOB and suctioning under direct vision. Alternatively, oxygen can be administered through the working channel and used to blow secretions out of the way. The additional benefit of the O2 insufflation technique is the increased FI O2 provided in spontaneously breathing patients. Switching back and forth between suction and O2 insufflation is often useful. Once the ETT is positioned approximately 3–4 cm above the carina, the FOB is removed. Difficulty in removing the FOB can result from a narrow nasal passage with crimping of the ETT, and also when the FOB is inadvertently passed through the Murphy eye of the ETT, trapping it in place. If this occurs, the fiberoptic bronchoscope and the ETT may have to be removed as a unit and the procedure begun once again. Oral Technique The FOB can be advanced through the oropharynx in both awake, spontaneously ventilating patients and those who are asleep and being ventilated with a mask or LMA. The sedation

Figure 2.34. Fiberoptic bronchoscope with endotracheal tube (ETT) threaded over the insertion end of the FOB. The 15-mm airway connector has been removed, and the ETT is secured to the body of the FOB with a piece of tape. The distal (insertion) end of the FOB is lubricated with a silicone-based fluid, the cuff of the ETT is deflated. The tip of the FOB can only be flexed in one plane. To maneuver the FOB in other planes the scope itself must be longitudinally twisted. (From Zupan J. Fiberoptic bronchoscopy in anesthesia and critical care. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: J. B. Lippincott Co., 1992, p 258; with permission.)

and local anesthesia preparation for an awake oral intubation is the same as that required for a nasal intubation. With oral intubation in a spontaneously ventilating patient, the FOB is advanced into the airway through a rigid plastic Ovassapian oral airway intubator (Figure 2.36A). The oral intubation can be more difficult in some patients because the FOB must take a more acute bend at the oropharynx in order to be directed toward the larynx compared with the more gentle curvature required for nasal intubation. Having an assistant perform a jaw-thrust or chin-lift maneuver may be helpful in this regard. When FOB-assisted intubation is performed in patients under general anesthesia, concomitant ventilation can be achieved using an LMA, Intubating Fastrach™ LMA, or the Patil intubating mask with self-sealing diaphragm (Figure 2.36B) along with the Ovassapian oral airway intubator, as described by Rogers and Benumof [31]. Entry into the glottis is generally easier with an LMA-FOB-assisted intubation than with an intubating mask-FOB-assisted technique. D I F F I C U LT A I RWAY A L G O R I T H M S The ASA Difficult Airway Algorithm Practice guidelines for management of the difficult airway were originally published in 1993 [6], and were updated in 2003 by the ASA Task Force on Management of the Difficult Airway [12]. The original practice guidelines (1993) were developed by a taskforce of ASA members who expounded on the original ideas put forth in a medical intelligence article written by J. L. Benumof in 1991, entitled Management of the Difficult Airway [5].

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Figure 2.35. View of the larynx and carina via a FOB. This figure demonstrates the normal anatomy of the larynx (A) as well as the view obtained from a FOB positioned just above the laryngeal inlet (B). After passage of the FOB through the vocal cords and down the trachea the carina comes into view (C). The tracheal cartilages are c-shaped and are joined posteriorly with a membrane. This anatomy allows for identification of the various portions of the tracheal bronchial tree. (From Zupan J. Fiberoptic bronchoscopy in anesthesia and critical care. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: J. B. Lippincott Co., 1992, p 260; with permission.)

Figure 2.36. The oral airway intubator and the intubating anesthesia mask. The oral airway intubator (A) has a channel large enough to pass an 8.0-mm ETT. The intubating anesthesia mask fits normally over the patient’s face and is equipped with the usual 15-mm airway connector. In addition, the intubating anesthesia mask contains an intubating port with self-sealing diaphragm through which a FOB and previously threaded ETT may pass (B). The scope passes via the intubating port through the intubating oral airway and then into the trachea. The ETT (previously threaded over the bronchoscope) is then advanced into the trachea. The bronchoscope is withdrawn, the ETT is grasped near the patient’s mouth and the anesthesia mask is removed with care not to pull the ETT out of the trachea in the process. (From Zupan J. Fiberoptic bronchoscopy in anesthesia and critical care. In Benumof JL, ed. Clinical Procedures in Anesthesia and Intensive Care. Philadelphia, PA: J. B. Lippincott Co., 1992, p 261; with permission.)

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In 1996, Benumof wrote another landmark article discussing the development and use of the LMA and its implications for the ASA algorithm [14]. This article contributed to the ASA’s decision to revise the 1993 algorithm. The current version emerged after the ASA Task Force reviewed the literature published over the past 60 years and obtained expert opinions from other ASA members to build a consensus. The 2003 Practice Guidelines Key Points are summarized in Table 2.8. Several critical decision tree elements are present in the ASA difficult airway algorithm. These include recognition of the difficult airway, awake intubation techniques, and anesthetized intubation techniques. Figure 2.37B shows the ASA algorithm as revised in 2003, along with modifications (in red) as required for utilization in the trauma patient. Recognition of the Difficult Airway The ASA algorithm begins with recognition of airway difficulty. Penetrating trauma to the neck with stridor and cyanosis is easily recognized as a potentially difficult airway. However, more subtle anatomic or pathologic causes of airway difficulty can go unrecognized in the traumatized patient because of hasty preoperative evaluation or preoccupation with other aspects of care. Missed signs of a difficult airway can be minimized if one looks carefully for both pathologic and anatomic abnormalities. Whenever the patient is recognized to have a difficult airway, the clinician should consider securing the airway by using an awake technique, as long as the patient is cooperative, hemodynamically stable, and spontaneously ventilating. Awake Limb of the ASA Difficult Airway Algorithm After deciding to intubate the trachea by using an awake technique, the airway expert must select the most appropriate technique given the reason for airway difficulty and the clinical circumstances. The technique chosen is not as important as is the airway expert’s experience and judgment as to suitability of a particular airway intubation technique given the patient’s difficult airway circumstances. Indeed, the ASA algorithm does not endorse any specific airway technique. However, it does emphasize that the patient must be properly prepared for an awake technique, and the physician must ensure that spontaneous ventilation continues and O2 saturation is maintained throughout the procedure. In trauma scenarios, the patient must also be cooperative and stable. The basic ASA algorithm recommends considering abandoning the airway attempt while maintaining spontaneous ventilation, and allowing the patient to recover from topicalization or sedative medications and resume management later with a better plan. However, stopping is rarely an option in emergency airway management situations. If at any time during the awake intubation manipulation, the patient is unable to ventilate by mask and intubation is not successful, then consideration should be given to use of emergency airway adjunct devices such as the LMA, Combitube, TTJV, or a surgical airway. Uncooperative/Unstable/“Anesthetized” Limb of the Algorithm The physician may be confronted with the need to intubate the trachea of an unconscious or anesthetized patient with a

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difficult airway, which was elaborated on earlier. In the uncooperative patient, preinduction assessment should have identified factors that might make intubation of the trachea difficult and the airway expert should consider using a technique that maintains spontaneous ventilation despite the need for anesthesia. ASA Difficult Airway Algorithm Modified for Trauma Trauma patients, who are hemodynamically stable without specific injuries to the head, neck, maxilla-face, or chest, can be managed as outlined by the ASA algorithm (Figure 2.37B). Isolated abdominal or extremity injuries in hemodynamically stable patients fall into this category. However, in this “uncomplicated” setting, the anesthesiologist must maintain a heightened vigilance for and undertake protective measures against aspiration (Table 2.9). Trauma and associated conditions such as apprehension, opioid administration, alcohol ingestion, and gastrointestinal disorders are all associated with an increased volume of gastric contents. Pain, trauma, and apprehension decrease the gastric pH and further increase the risk that passive regurgitation will progress to aspiration syndrome. Therefore, all trauma patients are expected to have full stomachs, and an RSI technique of intubation should always be considered (see Chapter 9). However, many airway disasters have resulted from an inappropriate placement of gastric regurgitation and pulmonary aspiration on a hierarchical level above airway difficulty. Thus, the clinician must always fully evaluate the airway. If the patient has an anticipated difficult airway, the trachea should be intubated by using an awake technique. Despite the increased risk of aspiration in these trauma patients, awake techniques can be safely used provided the physician maintains close observation of the patient’s mental status. If the patient is awake and following commands, then the patient’s airway protective mechanisms should be functional. Indeed, Ovassapian and colleagues intubated the tracheas of 123 patients considered to be at high risk for aspiration of gastric contents by using an awake technique. Regurgitation occurred in only one patient, and no patients suffered aspiration [32]. Therefore, the ASA algorithm can be followed without significant modification in patients with isolated extremity or abdominal injuries with documented absence of cervical spine, brain, neck, maxillofacial, or chest injury. Previously, the traditional overriding goal in securing a difficult airway in patients with a full stomach was the prevention of catastrophic aspiration. It is now more clearly understood that preventing hypoxia and brain injury is most important. The general principles of the ASA algorithm as they apply to the trauma airway are outlined in Figure 2.37. The modifications of the algorithm for trauma as compared with the general algorithm are summarized in Table 2.9. First, stopping to come back another day is seldom an option with trauma. Second, an awake ETT technique should be chosen in a difficult airway patient providing the patient is cooperative, stable, and spontaneously ventilating. Third, if the patient becomes uncooperative/combative or unstable, then sedative drugs may need to be administered to gain control. However, if the airway is deemed difficult, spontaneous ventilation should be maintained, if possible. Finally, a surgical airway may be the best choice in certain conditions.

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Table 2.8: Principles of the ASA Difficult Airway (DA) Algorithm Principles

Examples / Comments

A. Airway history is useful B. Airway examination (11 step)

Ask patient, check chart/bracelet Should be conducted on all patients whenever feasible (Table 2.3). e.g., rheumatoid arthritis patients may need flexion/extension C-spine x-rays

C. Additional evaluation may be indicated in some patients D. Basic preparation for a difficult airway, per 2003 ASA DA Guidelines E. When a patient is identified as having a DA several things should happen:

F. The anesthesiologist should have a strategy for DA management – one such strategy is following the algorithm (See algorithm, Figures 2.37B–2.42)

G. The anesthesiologist should also have a strategy for extubation or tube change of the DA patient. Every DA extubation strategy requires consideration of the following four elements:

H. Follow-up care and documentation

Requires a portable DA storage unit with contents that include airway tools that can assist management of the difficult airway (Table 2.1). 1. Inform patient / family of risks, plans, and alternate management methods 2. Identify an experienced helper to assist in managing the DA 3. Preoxygenate 4. Pursue opportunities to administer O2 to patient during DA management 1. Assess the likelihood of any one of the four basic problems: –Difficult ventilation –Difficult intubation –Difficulty with patient cooperation or consent –Difficult tracheostomy 2. Consider the merits of crossing the three basic bridges to airway access: –Awake vs. general anesthesia (RSI +/– modified with PPV) –Natural airway with endotracheal tube (ETT) vs. surgical airway –Spontaneous ventilation vs. apnea 3. Identify the preferred primary approach (patient and condition specific) 4. Identify a back-up approach (i.e., Plan “B”). 5. Exhaled CO2 should be used for confirmation of tracheal intubation 6. Consideration of conducting surgery with regional/local technique. Significant judgment is required. Regional is seldom a wise choice for acute polytrauma patients (Table 2.6). 1. Relative merits of awake extubation. 2. Factors that may have an adverse impact on ventilation after extubation 3. Formulate an airway management plan that can be implemented if the patient is unable to maintain adequate ventilation after extubation 4. Consider use of an AEC for short-term use. An AEC can serve as a guide for expedited reintubation, or (via the hollow inner core) as a method to provide O2 by insufflation (if patient breathing spontaneously) or via jet ventilation. 1. Inform patient/family of difficulty. Suggest patient get a card in wallet and a bracelet stating difficult airway 2. Document in chart specific problems with mask ventilation, LMA ventilation, or intubation. Also, document which tools were used successfully or unsuccessfully. Provide all guidance relevant for the next person managing the patient in the future.

ASA, American Society of Anesthesiologists; DA, difficult airway; O2 , oxygen; RSI, rapid sequence induction; PPV, positive pressure ventilation; ETT, endotracheal tube; CO2 , carbon dioxide; AEC, airway exchange catheter; LMA, laryngeal mask airway.

Five Common Trauma Difficult Intubation Scenarios Traumatic Brain Inury (TBI)/Intoxication In the setting of TBI, surgical decompression/evacuation is frequently the primary intervention required for resolution of increased intracranial pressure (ICP). Endotracheal intubation and subsequent modest hyperventilation constitute important temporizing modalities (Figure 2.38). Hyperventilation serves to decrease cerebral blood flow by causing cerebral vasoconstriction via an increase in intracellular brain pH (see Chap-

ter 11). Simultaneously, maintenance of mean arterial pressure (MAP) in a normal or slightly elevated level throughout these manipulations is important to maintain cerebral perfusion pressure (CPP = [MAP – ICP]). Patients with a CPP less than 60 mmHg have a worse outcome for similar categories of head injury and the Glasgow Coma Scale score than patients with normal CPP [33], and a CPP more than 70 mmHg is desirable if it can be accomplished [34]. Airway management considerations for the TBI patient begin with a determination of acuity followed by airway

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Summary of the ASA Difficult Airway Algorithm Modifications for Trauma (Review with Figure 2.37A) A. Stopping to come back another day is seldom an option with trauma B. A surgical airway may be the first/best choice in certain conditions C. An awake ETT technique should be chosen in a DA patient providing the patient is cooperative, stable, and spontaneously ventilating. D. If the patient becomes uncooperative/combative general anesthesia (GA) may need to be administered—but if the airway is difficult, spontaneous ventilation (SV) should be continued (if possible). E. Awake limb of the ASA Algorithm—Trauma Notes. An awake intubation technique is recommended for all trauma patients with a recognized difficult airway…. Providing the patient is cooperative, stable, and maintains spontaneous ventilation and adequacy of O2 saturation. The ASA DA Algorithm does not endorse any particular airway technique. However, it does emphasize that the patient must be properly prepared (mentally and physically) for an awake technique. F. Anesthetized or uncooperative limb of ASA DA Algorithm—Trauma Notes. There are three common conditions when the need arises to intubate the trachea of an unconscious or anesthetized trauma patient with a DA: 1. Clinician fails to recognize a difficult airway in preoperative evaluation prior to the induction of anesthesia 2. The DA patient is already unconscious prior to being assessed by the trauma anesthesiologist 3. The patient obviously has a DA, but is hemodynamically unstable (e.g., following trauma) or absolutely refuses to cooperate with an awake intubation (e.g., child, mentally retarded, drugged, or head-injured adult). Once the patient is anesthetized or is rendered apneic or presents comatose and the trachea cannot be intubated, O2, enriched mask ventilation (MV) is attempted. If MV adequate, a number of intubation techniques may be employed. Techniques allowing continuous ventilation during airway manipulations are favored over those requiring an interruption of MV (e.g., FOB, via an LMA or an airway intubating mask, with self-sealing diaphragm). Alternatively, techniques requiring a cessation of ventilation (at least temporarily) can be employed. These techniques are relatively contraindicated for patients with large right-toleft transpulmonary shunt, or decreased FRC. G. Confirmation of endotracheal tube (ETT) position. Immediately after the patient's trachea is intubated, one must confirm ETT position with end-tidal CO2 measurement. If end-tidal CO2 measurement is unavailable, Wee's esophageal detector device (EDD) is reasonably reliable (close to 100% sensitive and specific). H. Extubation or ETT change of the DA. If the conditions that caused the airway to be difficult to intubate still exist at the time of extubation, or if new DA conditions exist (e.g., airway edema, halo), then the trachea should be extubated over an AEC and or with the assistance of a FOB. Figure 2.37B. (Continued ) ASA difficult airway algorithm, with modifications (in bold) required for trauma. The algorithm begins with recognition of the difficult airway. If the patient is recognized to have a difficult airway then the awake limb of the algorithm is followed. Whereas, if the patient is uncooperative, unstable, or was not recognized to have a difficult airway, the anesthetized limb is followed. Regardless of the technique used to secure a definitive airway, confirmation of mechanical ventilation with either end-tidal CO2 or other test is mandatory. The original algorithm is from Caplan RA. Practice Guidelines for Management of the Difficult Airway. Anesthesiology 2003;98:1273; with permission, along with modifications (in bold) as published in ASA Difficult Airway Algorithm modified for Trauma (Wilson WC. Trauma: airway management. ASA difficult airway algorithm modified for trauma – and five common trauma intubation scenarios. ASA Newsletter 2005;69(11):10; with permission.)

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Table 2.9: Modification of the ASA Difficult Airway (DA) Algorithm for Trauma Management Choices

Standard ASA DA Algorithm

Trauma ASA DA Algorithm

Unsuccessful intubation after general anesthesia induced

Awakening the patient is always an option

Awakening/stopping is seldom an option

Surgical airway decision

Invasive surgical airway is performed for failed intubation/failed ventilation

Surgical airway may be the first/best choice

Management of recognized difficult airway

Awake intubation

Awake intubation technique only if cooperative, stable, and spontaneously ventilating

Failed awake intubation

Cancel is an option

Uncooperative/combative patient requires general anesthesia with or without spontaneous ventilation

Regional for anesthetic management

Regional anesthesia is usually an option

Regional is occasionally an option

ASA DA, American Society of Anesthesiologists Difficult Airway Algorithm (see also Figure 2.37B, A–B).

evaluation. If the patient has a Glasgow Coma Score (GCS less than 9) airway management begins at the anesthetized limb of the ASA difficult airway algorithm just as in any unstable uncooperative patient. If the patient has stable hemodynamics, a GCS more than 9, and an airway that appears difficult to intubate, then an awake intubation technique should be considered. Cervical Spine Injury C-spine injury should be suspected in all trauma patients, especially those with a significant blunt mechanism of injury (i.e., front-end motor vehicle crash more than 35 miles per hour without seat belt), and those patients admitted with altered mental status [35, 36]. Because comatose patients cannot respond to a clinical examination, all head-injured and/or intoxicated patients, and others in whom a clinical exam cannot be performed must initially be assumed to have cervical instability. Few well controlled studies are available to guide airway management for these patients. However, several excellent reviews of C-spine injury and airway management exist [37–40]. When confronted with the patient with suspected C-spine injury, six points should be considered (Table 2.10). The Cspine airway management algorithm (Figure 2.39) follows directly from concepts outlined in Table 2.10. First, intubation of the proved or suspected C-spine injured patient is analogous to intubation of any other patient, except that there is an added handicap because the head and neck should not be moved. Second, the patient must have his or her airway evaluated for all the other factors that would predict a difficult airway. Third, outcome data indicate that there are no differences in terms of incidence of neurologic deficit between awake intubation and intubation under general anesthesia as long as the operator does not move the head on the neck [41, 42]. Fourth, if the C-spine is known or suspected to be unstable, and the patient is awake, cooperative, and otherwise stable, an awake intubation, optimally with a FOB, should be pursued because this allows for neurologic evaluation after intubation. Fifth, if intubation is contemplated for neck surgery in a patient with known C-spine injury, both awake intubation and awake positioning should be pursued. (see also Chapters 13 and 14). And finally,

consideration must be given to using an intubation technique that does not require head extension or the sniffing position to optimally expose the glottis and intubate the trachea, especially when dealing with the uncooperative/unstable/anesthetized limb of the difficult airway algorithm. In a landmark review of C-spine injury and airway management, Hastings mentions the occurrence of two cases of quadriplegia or death after laryngoscopy in patients with unrecognized C-spine injuries [38]. The vast majority of cervical motion during glottic visualization and intubation with conventional laryngoscopy using a Macintosh blade is produced at the occipito-atlantal and atlanto-axial joints [43]. The subaxial cervical segments are only minimally displaced. It is well known that immobilization of the C-spine results in a higher incidence of difficulty with visualization of the vocal cords when using conventional laryngoscopy. This is because optimal alignment of the airway axes requires a certain amount of cervical segmental and rotational motion, which is prevented by immobilization techniques. For example, Nolan and Wilson [22] showed that immobilization of the C-spine resulted in a 22 percent incidence of grade III views, and reduced the optimal view of the larynx in 45 percent of patients. Use of a gum elastic bougie is invaluable whenever a grade III view of the glottis is encountered. While performing direct laryngoscopy, the operator maintains adequate force to keep the epiglottis in view. The bougie is then introduced by the operator and gently advanced anteriorly under the epiglottis and into the trachea. Often, tracheal clicks will be felt. With the operator still maintaining laryngoscopic force, the assistant threads the ETT over the bougie. The ETT may need to be rotated 90◦ to facilitate its passage through the glottis. Intratracheal placement is confirmed with PET CO2 detection. Rigid fiberoptic laryngoscopy with anatomically shaped blades such as the Bullard laryngoscope and Wuscope are reliable techniques to visualize the glottis and intubate the trachea in patients with known or suspected C-spine trauma [45, 46]. Unlike conventional laryngoscopy, the Bullard and Wuscope devices do not require head and neck movement to obtain a Grade I view of the vocal cords [44–47]. Alternatively, the McCoy levering laryngoscope or Heine CL flex tip blade can be used. This is a modified Macintosh laryngoscope that has a

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Figure 2.38. ASA difficult airway algorithm applied to closed-head injury/intoxication. (Wilson WC. Trauma: airway management. ASA difficult airway algorithm modified for trauma – and five common trauma intubation scenarios. ASA Newsletter 2005;69(11):12; with permission.) GCS, Glasgow coma scale; RSI, rapid sequence intubation; CPP, cerebral perfusion pressure; PPV, positive pressure ventilation; ASA, American Society of Anesthesiologists.

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Figure 2.39. ASA difficult airway algorithm applied to cervical spine injury. (Wilson WC. Trauma: airway management. ASA difficult airway algorithm modified for trauma – and five common trauma intubation scenarios. ASA Newsletter 2005;69(11):13; with permission.) DA, difficult airway; SV, spontaneous ventilation; SCI, spinal cord injury; RSI, rapid sequence intubation; GA, general anesthesia; FOB, fiberoptic bronchoscopy; ASA, American Society of Anesthesiologists.

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Table 2.10: Airway Considerations for Patients with Known or Suspected Cervical Spine Injuries Cervical Spine Injury Considerations

Airway Manipulation Implications

Must not move the neck

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Concomitant airway risks

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Maintain in-line immobilization. Consider use of intubation technique other than conventional laryngoscopy (e.g., FOB, Bullard, Wuscope, McCoy blade, light wand, Glidescope) Routine use of gum-elastic bougie if rigid laryngoscopy technique chosen Other concerns similar to any other patient with no neck range of motion. Awake technique if otherwise high risk (HMD 70 mm Hg

3. Cervical spine injury:

C-spine airway algorithm (Figure 2.39) Awake technique if otherwise high risk (HMD 28◦ C) to prevent further hypothermia. Esophageal stethoscopes are helpful for listening to heart and breath sounds but also contain a temperature sensor. Of note, gastric suctioning will artifactually lower esophageal temperatures [72]. The distal esophagus is considered a core temperature measuring site as is the tympanic membrane, PA catheter sensor, and nasopharynx. Tympanic temperatures reflect brain temperature and are commonly employed with total circulation arrest for repair of the aorta. Intermediately accurate sites for temperature measurement are the bladder, rectum, mouth, and axilla. Skin temperatures are less helpful as they may reflect ambient temperatures and superficial vasoconstriction of the skin [73]. Neurologic Monitoring Traumatic brain injury is unfortunately frequent and frequently catastrophic (see Chapters 11 and 12). A good outcome from a trauma includes an excellent neurologic prognosis. However, in the trauma setting, sophisticated neurologic monitoring, beyond intracranial pressure monitoring, is not commonly utilized. Systemic monitoring can improve outcome by limiting secondary brain injury from hypotension and hypoxemia. Intracranial Pressure The skull contains brain tissue, blood, and cerebrospinal fluid. Autoregulation provides for a relatively stable flow of blood to the brain over a range of blood pressures (typically MAPs of 50–150 mmHg). For the brain-injured patient, autoregulation is disrupted and cerebral blood flow can change dramatically. This contributes to secondary brain injury. In addition, systemic hypotension and hypoxemia associated with the trauma can cause cytotoxic and vasogenic edema. Systemic monitors can assist in limiting hypotension and hypoxemia.

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By measuring the intracranial pressure (ICP), the anesthesiologist can track cerebral perfusion pressure (CPP = MAP – ICP) and optimize brain perfusion (see Chapter 12). Multiple maneuvers such as raising blood pressure, decreasing cerebral spinal fluid volume (drainage, decreased production via pharmacologic agents), decreasing brain swelling (osmotic diuresis, steroids) and upright positioning may be used to increase CPP. Treatment of intracranial hypertension should begin with pressure levels above 20 mmHg [74], though some would suggest above 15 mmHg [75]. The CPP goal should be approximately 60 mmHg. Levels below 50 mmHg are associated with poor outcome and aggressively treating a patient to raise CPP above 70 mmHg with pressors and fluids is associated with systemic morbidity such as acute respiratory distress syndrome (ARDS) [76]. ICP is most commonly measured supratentorially through a ventriculostomy or an intracranial “bolt.” A ventriculostomy is a catheter placed in the lateral ventricle, which is attached to a fluid-filled column and a pressure sensor. Through the catheter, cerebrospinal fluid may be drained, medications injected, and ICP measured. Thus, the ventriculostomy acts as a monitor and a therapeutic device. The bolt or screw is a hollow device placed in the subarachnoid space and attached to a pressure transducer or fiber optic cable. ICP can be measured but cerebrospinal fluid cannot be withdrawn. The bolt has a lower infection rate and is easier to place than the ventriculostomy. The Brain Trauma Foundation considers the ventricular catheter “the most accurate, low-cost and reliable method of monitoring intracranial pressure” [77]. Electroencephalogram (EEG) EEG monitoring records spontaneous electrical activity in the cerebral cortex. Electrodes are placed on the scalp in a standardized fashion. Waveforms are characterized by varying frequency and amplitude and the location in which the signal was obtained. Four basic frequencies are described: delta (0–4 Hz), theta (4–8 Hz), alpha (8–13 Hz), and beta (>13 Hz). Delta waves, which are slow, synchronized waves, are seen with deep anesthesia or sleep, but may also occur with ischemia or severe metabolic disturbances. An awake patient will usually have disorganized, more complex waveforms such as beta waves [78]. EEG monitoring is most commonly used for detecting seizure foci. Intraoperatively, EEG is frequently used to monitor cerebral ischemia during carotid surgery when one carotid artery is occluded. EEG has been used in the neurointensive care setting for patients with traumatic brain injury. It is used to detect subclinical seizure activity and to aid in prognosticating outcomes in traumatic brain injury patients. Studies of EEG in traumatic brain injury have shown that traumatic brain injury patients have a high risk of developing seizure activity, particularly older patients and those with baseline seizure disorders [79]. Bispectral Index (BIS) Interpreting raw EEG data in the operating room is cumbersome and a highly technical skill. Several monitors are available that convert select EEG signals into a single number that reflects the patient’s level of consciousness. The algorithm used to convert the raw EEG is guarded. This number is used to guide

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Table 5.9: MEP and SSEP Protocols in Use at the MetroHealth Medical Center Motor Evoked Potential (MEP) Monitoring Anesthesia Protocol Bolus of Midazolam as needed throughout the case No volatile agents (i.e., avoid Isoflurane, Sevoflurane, and Desflurane) 50–70% N2 O Continuous infusion of Propofol (75–300 μg · kg · min−1 ) Continuous infusion of Fentanyl or Remifentanil A single dose of neuromuscular relaxant for intubation A bite block must be placed prior to turning the patient prone to decrease the risk of tongue and lip lacerations Somatosensory Evoked Potential (SSEP) Monitoring Anesthesia Protocol 1–2 mg of Midazolam preop 0.5 MAC of Isoflurane, Sevoflurane, or Desflurane 50% N2 O Continuous infusion of Fentanyl or Remifentanil Neuromuscular blockade as needed

Somatosensory Evoked Potentials (SSEPs) The somatosensory system relays vibration, proprioception, and light touch information from the periphery to the central nervous system. Electrical stimuli are applied to peripheral nerves (most commonly median, ulnar, common peroneal, and posterior tibial) and signals are assessed along the path of the nerve to the cortex. Typically, electrical potentials are assessed at the level of the cortex by scalp electrodes. Many signals are averaged from repeated stimulation to obtain a clinically useful waveform [78]. SSEP signals are carried mostly in the posterior spinal column; thus, anterior damage may not be recorded by the SSEP. SSEPs are most commonly used during spinal surgery and thoracic aneurysm repair. Anesthetic agents have variable effects on the signal. Motor Evoked Potentials (MEPs) Transcranial or spinal cord electrical stimulation produces a descending signal the can be recorded over the spinal cord, peripheral nerve, or muscle. Damage to anterior spinal tracts (motor tracts) not identified by SSEPs might be recognized by MEPs. MEPs are sensitive to inhaled anesthetic agents, and a total intravenous anesthetic approach is commonly employed with muscle relaxant to prevent gross motor movement [85]. Cerebral Oximetry

pharmacologic therapy and depth of anesthesia. The BIS Monitor by Aspect is the most commonly used model. Specialized gel pads are placed on the patient’s forehead and attached to the corresponding monitor. The gel pad must be firmly attached to the patient as impedance will reduce signal quality. Patients may require muscle relaxation to obtain reliable processed EEG information because muscle activity can interfere with the interpretation of EEG signals. In trauma patients, depth of anesthesia monitors would be predicted to behave normally. The brain-injured patient potentially presents a special case. Several studies have taken place trying to correlate the Glasgow Coma Scale score and observational sedation scales with BIS levels in the brain-injured patient. A correlation exists between the Glasgow Coma Scale score and BIS so that the higher the Glasgow Coma Scale score, the higher the BIS. This relationship was maintained both with and without sedation, validating the use of anesthetic depth monitors in brain-injured patients [80, 81]. Of note, use of a processed EEG monitor does not guarantee lack of awareness as numerous case reports show [82, 83].

Evoked Potentials Evoked potentials measure nervous system electrical activity that has been elicited by a stimulus. Evoked potentials are described in terms of amplitude, latency, and morphology (see also Chapter 14). The most common evoked potentials used in the operating room are sensory and motor. Evoked potentials are not commonly employed during the initial trauma surgery. However, patients often return for definitive stabilization of injuries that are appropriate for evoked potential monitoring. As anesthetic agents can affect evoked potentials, protocols have been developed to provide optimal signal strength and interpretation. Sample guidelines from MetroHealth Medical Center in Cleveland, Ohio, are shown in Table 5.9 [84].

Over the past 10 years, the concept of measuring regional cerebral oxygen saturation has caught on. Cerebral oximetry can be measured both noninvasively with near-infrared spectroscopy, or invasively with a catheter placed in the jugular bulb to measure jugular bulb oxygen saturation (SjvO2 ). Venous blood from the brain drains into the jugular bulb located at the base of the skull. To measure jugular bulb saturation, a 4 Fr sheath is placed in the internal jugular vein and advanced cephalad. A catheter is placed through the sheath and into the jugular bulb located near the base of the skull. Placement is typically confirmed by radiography [86]. The catheter has an oximetric tip and measures the saturation of cerebral venous blood real time. In head trauma patients, the catheter is typically placed either on the ipsilateral side of injury or bilaterally [87]. Treatment can thus be tailored toward optimizing cerebral saturation. This can be done by therapeutic maneuvers geared toward improving cerebral blood flow, such as treating elevated ICP with mannitol, hyperventilation, and so on, or by using volume or vasoactive drugs to improve perfusion pressure (see also Chapters 11 and 12). There are multiple limitations to using jugular bulb monitoring. The procedure itself has multiple risks relating to central venous access, such as carotid puncture, hematoma, and pneumothorax. There is also the risk of infection and/or thrombosis. Also, the catheter must be placed properly in the jugular bulb. If it is not, the sample volume may contain both intracranial venous drainage and extracranial venous drainage, which can have a marked impact on interpretation [88]. A study performed in 2000 found that jugular bulb monitoring did not significantly influence the management of head trauma patients [89]. Many centers now use noninvasive near-infrared spectroscopy in place of jugular bulb catheters to evaluate cerebral oximetry. Regional cerebral saturation monitors use near-infrared spectroscopy, similar to pulse oximetry, to measure tissue

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MONITORING

saturation (rSO2 ). Regional cerebral saturation is measured noninvasively by using cutaneous patches placed on the forehead. The alteration of regional cerebral perfusion and thus rSO2 can be detected by the sensors. Cerebral oximetry is frequently used in the cardiac surgical population. Multiple studies have shown improvements in stroke rates and major organ morbidity and mortality when cerebral saturation is measured and interventions performed to keep the saturation within 75% of baseline [90]. Cerebral oxygen saturation can be improved by improving cardiac output, FiO2 , increasing hematocrit, or increasing pCO2 . Cerebral oximetry is also useful in the trauma patients. Cerebral blood flow depends on CPP. Therapy in head trauma patients is guided toward improving CPP and thus cerebral perfusion in the setting of elevated ICP. In the past, many patients needed to have invasive ICP monitors placed in order to determine CPP. A study in 2002 showed, not surprisingly, a correlation of CPP to cerebral saturation. An rSO2 greater than 75% suggested CPP was adequate to meet metabolic demands, whereas rSO2 less than 55% suggested inadequate CPP [91]. A follow-up study showed a correlation of cerebral hypoxia (rSO2 ) less than 60% with lower Glasgow Coma Scale scores, lower CPP, more severe head computed tomography score, and decreased survival [92]. Cerebral oximetry monitoring may be useful in managing the trauma patient, offering a noninvasive measure of cerebral perfusion. Anesthetic interventions can be made in an effort to improve cerebral perfusion in the head trauma patient by using the rSO2 as an objective measure of the efficacy of intervention. Limitations of cerebral oximetry include effect of temperature on near-infrared absorption spectrum, contamination of the signal by chromophores in the skin, and differences between the various manufacturers’ devices. C O N C LU S I O N Standard monitoring, including auscultation of breath and heart sounds and secure venous access, is the cornerstone of any anesthetic technique for patients with trauma. Standard monitoring includes ECG, noninvasive blood pressure, pulse oximetry, PET CO2 , precordial or esophageal stethoscope, and core temperature. A peripheral nerve stimulator is used to assess degree of neuromuscular blockade. Invasive monitoring, including arterial line and CVP, is routine in seriously ill trauma patients. Arterial pulse contour analysis is useful to assess fluid responsiveness. Consideration should also be given to monitoring for awareness in trauma patients, as many patients have hemodynamic instability that limits their ability to tolerate sufficient anesthetic agents to blunt awareness and recall. Anesthetic outcomes have improved dramatically over the past few decades, in large part due to technological advances. Technology developed for primary use in other fields has found its way into perioperative use. While not all anesthesiologists will be well versed in every modality, a familiarity with options for monitoring and assessing patients is encouraged. Echocardiography is a rapid mode of assessing cardiac function and volume status (see Chapter 33). Doppler ultrasound, useful in locating blood vessels and assessing cerebral blood flow, is another technology that has a place in the trauma OR. Noninvasive arterial blood pressure monitoring and pulse wave analysis

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for cardiac output without a PA catheter are two technologies that are in clinical use but have not, as yet, found widespread acceptance. Monitors should improve outcome, not just add to the amount of information that must be interpreted and integrated by the anesthesia provider. In the increasingly mechanized operating room, the potential for distraction, false negatives, and equipment malfunction exists. According to ASA Closed Claims Analysis, however, most anesthesia machine malfunctions were user errors [93]. Electronic monitoring adds another dimension to the care we provide in the operating room. Although research may not validate improvement in patient outcomes, we believe clinical monitoring helps us avoid medical mismanagement. Having a wide array of monitors within easy reach does not absolve the clinician of utilizing clinical skills. The power of the physical exam: watching, listening, and laying hands on our patients has not yet been replaced. M U LT I P L E C H O I C E Q U E S T I O N S

1. Which of the following does NOT interfere with pulse oximetry readings? a. b. c. d. e.

Patient movement Dark nail polish Carboxyhemoglobin Deoxyhemoglobin Deeply pigmented skin

2. The carbon dioxide pressure gradient from arterial to endtidal increases under general anesthesia to what level? a. b. c. d. e.

1–3 mmHg 5–10 mmHg 15–20 mmHg 40–50 mmHg 95–100 mmHg

3. Elevated carbon dioxide levels caused by increased production of carbon dioxide can be attributed to all of the following except: a. b. c. d. e.

Malignant hyperthermia Cancer Coma Fever Burn

4. Low-pressure alarms are caused by which factor: a. b. c. d. e.

Breathing circuit disconnect Dyssynchronous ventilation Disconnect from wall oxygen Reduced lung compliance Endotracheal tube obstruction

5. Information obtained from a PA catheter includes all of the following except: a. Cardiac output b. Central venous pressure

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c. Pulmonary artery pressure d. Left ventricular volume e. Pulmonary artery wedge pressure 6. A falsely low mixed venous oxygen measurement will occur in which condition? a. b. c. d. e.

Sample taken in “wedged” position Mitral regurgitation Left-to-right intracardiac shunt AV fistula Sample taken in the cardiac sinus

7. Blood gas analysis provides information about the following except: a. b. c. d. e.

Oxygenation Cardiac function Ventilation Cellular metabolism Electrolytes

8. Interference with processed EEG signals (BIS) may occur by all of the following except: a. b. c. d. e.

Electromyography (EMG) activity Traumatic brain injury Dry gel High impedance Forehead surgery

9. Neurologic monitoring does not include: a. b. c. d. e.

Doppler Processed EEG ICP measurements End-tidal gas analysis Peripheral nerve stimulator

10. Most anesthesia machine malfunctions are due to: a. b. c. d. e.

User error Gas pressure failure False negatives Obstruction of oxygen flow meter Failure of proportioning system

ANSWERS

1. 2. 3. 4.

d b c a

5. d 6. e 7. b

8. b 9. d 10. a

REFERENCES

1. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring, Approved by the ASA House of Delegates on October 21, 1986, and last amended on October 25, 2005. www.asahq.org.

2. Australian and New Zealand College of Anaesthetists. Recommendations on monitoring during anesthesia. ANZCA Professional Document PS18, 2000. www.medeserv.com.au/anzca. 3. Royal College of Anaesthetists. Guidelines for the provision of anaesthetic services, 1999. www.rcoa.ac.uk. 4. Cheney FW. Changing trends in anesthesia-related death and permanent brain damage. ASA Newsletter 2002;66:6–8. 5. Webb RK, van der Walt JH, Runciman WB, Williamson JA, Cockings J, Russell WJ and Helps S. The Australian Incident Monitoring Study. Which monitor? An analysis of 2000 incident reports. Anesth Intensive Care 1993;21:529–42. 6. Tremper K, Barker S. Monitoring of oxygen. In Lake CL, Hines RL, Blitt CD. Ed. Clinical Monitoring: Practical Applications for Anesthesia and Critical Care. Philadelphia: W. B. Saunders, 2001, p 324. 7. Moller JT, Pedersen T, Rasmussen LS, Jensen PF, Pedersen BD, Ravlo O, Rasmussen NH, Espersen K, Johannessen NW, Cooper JB, et al. Randomized evaluation of pulse oximetry in 20,802 patients: I. Design, demography, pulse oximetry failure rate, and overall complication rate. Anesthesiology 1993;78:436–44. 8. Moller JT, Johannessen NW, Espersen K, Ravlo O, Pedersen BD, Jensen PF, Rasmussen NH, Rasmussen LS, Pedersen T, Cooper JB, et al. Randomized evaluation of pulse oximetry in 20,802 patients: II. Perioperative events and postoperative complications. Anesthesiology 1993;78:445–53. 9. Cote CJ, Rolf N, Liu LM, Goudsouzian NG, Ryan JF, Zaslavsky A, Gore R, Todres TD, Vassallo S, Polaner D, et al. A single-blind study of combined pulse oximetry and capnography in children. Anesthesiology 1991;74:980–7. 10. Barker SJ. Recent developments in oxygen monitoring. ASA Annual Meeting Refresher Course Lectures. 2006;320:1–6. 11. Shelley K, Shelley S. Pulse oximeter waveform: photoelectric plethysmography. In Lake CL, Hines RL, Blitt CD, ed. Clinical Monitoring: Practical Applications for Anesthesia and Critical Care. Philadelphia: W. B. Saunders, 2001, p 427. 12. Al-Shaikh B, Stacey S. Essentials of Anaesthetic Equipment, 2nd edition. London: Churchill Livingstone, 2002, p 117. 13. Venkatesh B, Clutton Brock TH, Hendry SP. A multiparameter sensor for continuous intra-arterial blood gas monitoring: A prospective evaluation. Crit Care Med 1994;22:588–94. 14. Coule LW, Truemper EJ, Steinhart CM, Lutin WA. Accuracy and utility of a continuous intra-arterial blood gas monitoring system in pediatric patients. Crit Care Med 2001;29:420–6. 15. Myles PS, Buckland MR, Weeks AM, Bujor M, Moloney J. Continuous arterial blood gas monitoring during bilateral sequential lung transplantation. J Cardiothorac Vasc Anesth 1999;13:253–7. 16. Eichorn JH. Standards for patient monitoring during anesthesia at Harvard Medical School. J Am Med Assoc 1986;256:1017–20. 17. Barker L, Webb RK, Runciman WB, Van der Walt JH. The Australian Incident Monitoring Study. The oxygen analyzer: Applications and limitations – an analysis of 200 incident reports. Anaesth Intensive Care 1993;21:570–4. 18. Tremper K, Barker S. Monitoring of oxygen. In Lake CL, Hines RL, Blitt CD, ed. Clinical Monitoring: Practical Applications for Anesthesia and Critical Care. Philadelphia: W. B. Saunders, 2001, p 315–16. 19. Keeling CD, Whorf TP. Atmospheric CO2 records from sites in the SIO air sampling network. Trends: A Compendium of Data on Global Change. Carbon Dioxide Information Analysis Center, Oak Ridge National Laboratory, U.S. Department of Energy, Oak Ridge, TN, 2005.

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MONITORING 20. Gravenstein J, Paulus D, Hayes T. Capnometric Methods: Gas Monitoring in Clinical Practice, 2nd edition. Boston: Butterworth-Heinemann, 1995, p 17. 21. Barash P, Cullen B, Stoelting, R. Clinical Anesthesia, 5th edition. Philadelphia: Lippincott, Williams & Wilkins, 2006, p 670. 22. Davis P, Kenny G. Basic Physics and Measurement in Anaesthesia, 5th edition. New York: Butterworth Heinemann, 2003, p 214. 23. Campbell FA, McLeod ME, Bissonnette B, Swartz JS. End tidal carbon dioxide measurement in infants and children during and after general anesthesia. Can J Anaesth 1994;41:107–10. 24. Eichhorn JH, Cooper JB, Cullen DJ, Maier WR, Philip JH, Seeman RG: Standards for patient monitoring during anesthesia at Harvard Medical School. J Am Med Assoc 1986:256:1017–20. 25. Eichhorn JH. Prevention of intraoperative anesthesia accidents and related severe injury through safety monitoring. Anesthesiology 1989;70:572–7. 26. Croswell RJ, Dilley DC, Lucas WJ, Vann WF Jr. A comparison of conventional versus electronic monitoring of sedated pediatric dental patients. Pediatr Dent 1995;17:332–9. 27. Cote CJ, Liu LM, Szyfelbein SK, Firestone S, Goudsouzian NG, Welch JP, Daniels AL. Intraoperative events diagnosed by expired carbon dioxide monitoring in children. Can Anaesth Soc J. 1986;33:315–20. 28. Baraka AS, Aouad MT, Jalbout MI, Kaddoum RN, Khatib MF, Haroun-Bizri ST. End-tidal CO2 for prediction of cardiac output following weaning from cardiopulmonary bypass. J Extra Corpor Techno 2004;36(3):255–7. 29. Ornato JP, Garnett AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med 1990;19(10):1104–6. 30. Manecke GR Jr, Popper PJ. Esophageal stethoscope placement depth: Its effect on heart and lung sound monitoring during general anesthesia. Anesth Analg 1998;86:1276–9. 31. Klepper ID, Webb RK, Van der Walt JH, Ludbrook GL, Cockings J. The Australian Incident Monitoring Study. The stethoscope: applications and limitations – an analysis of 2000 incident reports. Anaesth Intensive Care 1993;21:575–8. 32. Watson A, Visram A. Survey of the use of oesophageal and precordial stethoscopes in current paediatric anaesthetic practice. Paediatr Anaesth 2001;11:437–42. 33. Prielipp RC, Kelly JS, Roy RC. Use of esophageal or precordial stethoscopes by anesthesia providers: are we listening to our patients? J Clin Anesth 1995;7:367–72. 34. Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia, 3rd edition. Philadelphia: Lippincott-Raven Publishers, 1997, pp 194– 200. 35. Kaye P, O’Sullivan, I. Myocardial contusion: Emergency investigation and diagnosis. Emerg Med J 2002;19:8–10. 36. Potkin RT, Werner JA, Trobaugh GB, et al. Evaluation of noninvasive tests of cardiac damage in suspected cardiac contusion. Circulation 1983;66(3):627–33. 37. Wittebole X, Hantson P. Electrocardiographic changes after head trauma. J Electrocardiol 2005;38:77–81. 38. Shah N, Bedford RF. Invasive and noninvasive blood pressure monitoring. In Lake C, Hines R, Blitt C, ed. Clinical Monitoring: Practical Applications for Anesthesia and Critical Care. Philadelphia: W. B. Saunders, 2001, pp 181–203. 39. Janelle GM, Gravenstein N. An accuracy evaluation of the T-Line Tensymeter versus conventional invasive radial artery monitoring in surgical patients. Anesth Analg 2006;102:484–90.

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40. Belani K, Ozaki M, Hyson J, Hartmann T, Reyford H, Martino JM, Poliac M, Miller R. A new non invasive method to measure blood pressure. Anesthesiology 1999;91(3):686–92. 41. Duan Y, Smith CE, Como JJ. Cardiothoracic trauma. In Wilson WC, Grande CM, Hoyt DB, ed. Trauma Emergency Resuscitation Perioperative Anesthesia Surgical Management. New York: Informa Healthcare, 2007, Chapter 25, pp 469–99. 42. Levy JH, Yegin A. Anaphylaxis. What is monitored to make a diagnosis? Anesthesiol Clin N Am 2001;19:705–15. 43. Palter MD, Cortes V. Secondary triage of the trauma patient. In Civetta JM, Taylor RW, Kirby RR, ed. Critical Care, 3rd edition. Philadelphia: Lippincott-Raven, 1997, pp 1045–63. 44. Morgan BC, Martin WE, Hornbein TF, Crawford EW, Guntheroth WG. Hemodynamic effects of positive pressure ventilation. Anesthesiology 1966;27:584–90. 45. Jardin F, Delorme G, Hardy A, A Uvert B, Beuchet A, Bourdarias JP. Reevaluation of hemodynamic consequences of positive pressure ventilation: Emphasis on cyclic right ventricular afterloading by mechanical lung inflation. Anesthesiology 1990;72: 966–70. 46. Jardin F, Farcot JC, Gueret P, Prost JF, Ozier Y, Bourdarias JP. Cyclical changes in arterial pulse pressure during respiratory support. Circulation 1983;68:266–74. 47. Michard F, Teboul JL. Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation. Crit Care 2000;4:282–9. 48. Teboul J, Besbes M, Andrivet P, Axler O, Douguet D, et al. A bedside index assessing the reliability of pulmonary occlusion pressure measurements during mechanical ventilation with positive end expiratory pressure. J Crit Care 1995:7;22–9. 49. Robotham JL, Cherry D, Mitzner J, Rabson L, Lixfeld W, Bromberger-Barnea B. A re-evaluation of the hemodynamic consequences of intermittent positive pressure ventilation. Crit Care 1983;11:783–93. 50. Coriat P, Vrillon M, Perel A, Baron JF, et al. A comparison of systolic pressure variations and echocardiographic measurements of end-diastolic left ventricular size in patients after aortic surgery. Anesth Analg 1994:78;46–53. 51. Kramer A, Zygun D, Hawes H, Easton P, Ferland A. Pulse pressure variation predicts fluid responsiveness following coronary artery bypass surgery. Chest 2004;126(5):1563–68. 52. Tavernier B, Makhotine O, Lebuffe G, Dupont J, Scherpereel P. Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology 1998;89(6):1313–21. 53. Perel A, Pizov R, Cotev S. The systolic pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage. Anesthesiology 1987;67: 498–502. 54. Rooke GA, Schwid HA, Shapira Y. The effects of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during spontaneous mechanical variation. Anesth Analg 1995;80:925–32. 55. Preisman S, DiSegni E, Vered Z, Perel A. Left ventricular preload and function during graded hemorrhage and retransfusion in pigs: analysis of arterial pressure waveform and correlation with echocardiography. Br J Anaesth 2002;88:716–18. 56. Berkenstadt H, Friedman Z, Preisman S, Keidan I, Livingstone D, Perel A. Pulse pressure and stroke volume variations during severe haemorrhage in ventilated dogs. Br J Anaesth 2005;94(6):721–6.

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57. Ornstein E, Eidelman L, Drenger B, Elami A, Pizov R. Systolic pressure variation predicts the response to acute blood loss. J Clin Anesth 1998;10:137–40. 58. Reuter DA, Goepfert MSG, Goresch T, Schmoeckel M, Kilger E, Goetz AE. Assessing fluid responsiveness during open chest conditions. Br J Anaesth 2005;94(3):318–23. 59. Mark JB. Monitoring with CVP and PAC. ASA Annual Meeting Refresher Course Lectures. 2006;322;1–6. 60. Varon AJ. Arterial, central venous, and pulmonary artery catheters. In Civetta JM, Taylor RW, Kirby RR, ed. Critical Care, 3rd edition. Philadelphia: Lippincott-Raven, 1997. pp 847–65. 61. Moomey CB, Fabia TC, Croce MA, et al. Determinants of myocardial performance after blunt chest trauma. J Trauma 1998;45:988–96. 62. Rhodes A, Bennet ED. Early goal directed therapy: an evidencebased review. Crit Care Med. 2004;32:S448–50. 63. Kumar A, Anel R, Bunnell E, et.al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004;32:691–9. 64. Thys D, Hillel Z, Schwartz AJ. Textbook of Cardiothoracic Anesthesiology. New York: McGraw–Hill Companies, pp 632–37. 65. Sandham JD, Hull RD, Brant RF. A randomized controlled trial of the use of pulmonary artery catheters in high risk surgical patients. N Engl J Med 2003;348(1):5–14. 66. Shah MR, Hasselblad V, Stevenson LW. Impact of pulmonary artery catheters in critically ill patients: meta analysis of randomized controlled trials. J Am Med Assoc 2005;294(13): 1664–70. 67. Bishop MH, et al. Prospective randomized trial of survivor values of cardiac index, oxygen delivery, and oxygen consumption as resuscitation endpoints in severe trauma. J Trauma 1995;38(5):780–7. 68. Friese RS, Shafi S, Gentilello LM. Pulmonary artery catheter use is associated with reduced mortality in severely injured patients. Crit Care Med 2006;34(6):1597–1601. 69. Otto CM. Textbook of Clinical Echocardiography, 2nd edition. St Louis: W. B. Saunders, 2000, pp 59–79. 70. Tisherman SA. Clinical Practice Guideline: Endpoints of Resuscitation. Eastern Association for the Surgery of Trauma. www.east.org 71. Sessler D. Mild perioperative hypothermia. N Engl J Med 1997;336:1730–7. 72. Nelson EJ, Grissom TE. Continuous gastric suctioning decreased measured esophageal temperature during general anesthesia. J Clin Monit 1996;12:429–32. 73. Cork RC, Vaughan RW, Humphrey LS. Precision and Accuracy of Intraoperative temperature monitoring. Anesth Analg 1983;62:211–14. 74. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. Intracranial pressure thresholds. J Neurotrauma 2007;24(Suppl 1): S55–S8. 75. Saul TG, Ducker TB. Effects of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982;56:498–503.

76. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. Cerebral perfusion thresholds. J Neurotrauma 2007;24(Suppl 1):S59–S64. 77. Intracranial Pressure Monitoring Technology. J Neurotrauma 2007;24(Suppl 1):S45–54. 78. Mahla M. Neurologic monitoring. In Cucchiara RF, ed. Clinical Neuroanesthesia. New York: Churchill Livingstone, 1998, pp 125–76. 79. Ronne-Engstrom E, Winkler T. Continuous EEG monitoring in patients with traumatic brain injury reveals a high incidence of epileptiform activity. Acta Neurol Scand 2006;114:47–53. 80. Deogaonkar A, Gupta R, DeGeorgia M, Sabharwal V, Gopakumaran B, Schubert A and Provencio JJ. Bispectral Index monitoring correlates with sedation scales in brain-injured patients. Crit Care Med 2004;32:2545–6. 81. Paul DB, Umamaheswara Rao GS. Correlation of bispectral index with Glasgow coma score in mild and moderate head injuries. J Clin Monit Comput 2006;20:399–404. 82. Bevacqua B, Kazdan D. Is more information better? Intraoperative recall with a Bispectral Index Monitor in place. Anesthesiology 2003;99:507–8. 83. Mychaskiw G, Horowitz M, Sachdev V, Heath BJ. Explicit intraoperative recall at a bispectral index of 47. Anesth Analg 2001; 92:808–9. 84. Lovich-Sapola J. SSEP and MEP Monitoring Anesthesia Protocol. Personal communication. 85. Mahla M, Black S, Cucchiara RF. Neurologic monitoring. In Miller R, ed. Miller’s Anesthesia. Philadelphia: Elsevier, 2005, pp 1511–550. 86. Coplin WM, O’Keefe GE, Grady MS, Grant GA, et al. Thrombotic, infectious, and procedural complications of the jugular bulb catheter in the intensive care unit. Neurosurgery 1997;41(1):101–9. 87. Andrews PJD, Dearden NM, Miller JD. Jugular bulb cannulation: Description of a cannulation technique and validation of a new continuous monitor. Br J Anaesth 1991;67:553–8. 88. Edmonds HL. Pro: All cardiac surgical patients should have intraoperative cerebral oxygenation monitoring. J Cardiothorac Vasc Anesth 2006;20:445–9. 89. Latronico N, Beindorf AE, Rasulo FA, Febbrari P, et al. Limits of intermittent jugular bulb oxygen saturation monitoring in the management of severe head trauma patients. Neurosurgery 2001;48(2):454–6. 90. Murkin JM, Adams SJ, Novick RJ, et al. Monitoring brain oxygen saturation during coronary bypass surgery: A randomized, prospective study. Anesth Analg 2007;104:51–8. 91. Dunham CM, et al: Correlation of noninvasive cerebral oximetry with cerebral perfusion in the severe heads injured patient: A pilot study. J Trauma 2002;52(1):40–6. 92. Dunham CM, Ransom KJ, Flowers LL, et al. Cerebral hypoxia in severely brain injured patients is associated with admission Glasgow Coma Score, CT severity, cerebral perfusion pressure, and survival. J Trauma 2004;56(3):482–91. 93. Caplan RA, Vistica MF, Posner KL, Cheney FW. Adverse anesthetic outcomes arising from gas delivery equipment: A closed claims analysis. Anesthesiology 1997;87:741–8.

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Maxim Novikov and Charles E. Smith Objectives 1. Understand the timing, extent, and the immediate goals for the initial fluid resuscitation in trauma victims, individualized to specific patients. 2. Review the factors influencing choice of fluid for the initial and ongoing resuscitation. 3. Discuss factors influencing the decision for initiating transfusion therapy, choice of blood products, immediate and delayed risks and benefits of transfusion therapy. 4. Become familiar with the current state of therapies intended for the most severely injured patients, including recombinant factor VIIa and massive blood transfusion protocols.

Initial evaluation of an acutely volume-depleted trauma patient will include a primary and secondary survey according to Advanced Trauma Life Support® protocol, an estimate of blood volume deficit (Table 6.1), rate of the ongoing blood loss, and an evaluation of cardiopulmonary reserve and coexisting hepatic or renal dysfunction [1]. The overriding priority of trauma management is to maintain or restore vital organ perfusion and oxygenation above critical levels at an early stage, and to restore perfusion and oxygenation to normal levels as soon as it becomes appropriate. This is best achieved by stopping the bleeding and repleting intravascular volume. Perfusion pressure and oxygenated blood flow to vital organs are important determinants of outcome. Management priorities in an acutely bleeding trauma patient include ventilation and oxygenation (see Chapter 2), assessment of perfusion, estimation of volume replacement requirements, establishment or verification of adequate intravenous (IV) access (see Chapter 4), measurement of blood pressure, placement of electrocardiogram (ECG), pulse oximeter and capnograph, and laboratory studies. Placement of an arterial line allows for continuous monitoring of systolic pressure, pulse pressure, and stroke volume variability (see Chapter 4). Monitoring of temperature, urine output, arterial blood gases, hemoglobin, hematocrit, electrolytes, and parameters of coagulation are routine in severely injured, mechanically ventilated patients. Consideration is given to use of additional monitors (e.g., central venous catheter, pulmonary artery catheter, transesophageal echocardiography) and provision of anesthesia as needed. In the future, direct non-invasive monitoring of the target organ perfusion and oxygenation will become widely available and should be routinely used.

For induction of anesthesia in hemodynamically unstable patients, etomidate or ketamine are useful [2] (see Chapters 8 and 9) Titrated opioids, scopolamine, midazolam, and amnestic concentrations of volatile agents can then be used for maintenance of general anesthesia until the intravascular volume deficit has been corrected and bleeding is under control. Neuromuscular relaxants and other agents are given as clinically indicated [2]. T I M I N G A N D AG G R E S S I V E N E S S O F F LU I D R E S U S C I TAT I O N Aggressive fluid resuscitation aimed at earliest possible restoration of “normal” hemodynamics has been the mainstay of trauma management for years. However, in animal models of uncontrolled hemorrhage, this strategy uniformly leads to increased duration and volume of bleeding [3, 4] and decreased survival [3]. The proposed mechanisms include dilution of clotting factors, decreased blood viscosity, and blowout of hemostatic plugs with increasing blood pressure (Table 6.2). Hypotensive resuscitation, where the rate of fluid infusion is carefully titrated to a predetermined level of lower-than-normal blood pressure has been advocated in patients who are not pregnant and do not have traumatic head injury. The question of immediate versus delayed fluid resuscitation for hypotensive trauma patients was addressed in a landmark randomized clinical trial that demonstrated improved survival, shorter hospital stay, and less postoperative complications in patients who did not receive fluid resuscitation until arrival in the operating room [5]. The study was limited to isolated penetrating torso 101

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Table 6.1: Estimation of Blood Volume Deficit in Trauma

Table 6.2: Disadvantages of Immediate Fluid Resuscitation

Unilateral hemothorax

3,000 mL

Decreased blood viscosity

Hemoperitoneum with abdominal distension

2,000–5,000 mL

Blowout of hemostatic plug

Pelvic fracture

1,500–2,000 mL

Dilution of coagulation factors

Femur fracture

800–1,200 mL

Increased blood loss

Tibia fracture

350–650 mL

Delayed transport to definitive care

Smaller fracture sites

100–500 mL

injuries, and the receiving trauma center had a rapid response time such that most patients were in the operating room within one hour of injury. Benefits of delayed fluid resuscitation in the prehospital setting include minimal delay in transfer and surgical intervention and avoidance of increased blood pressure or hemodilution, which could disrupt the clot or alter resistance to flow around a partially formed thrombus. To date, no human study has shown detrimental effects of delayed or hypotensive resuscitation on survival, but so far the conclusive evidence on its superiority in trauma [6] or ruptured abdominal aortic aneurysm [7] is lacking. Consequently, in uncontrolled hemorrhagic shock, resuscitation is aimed at restoration of radial artery pulse, restoration of mental function, and a systolic blood pressure (SBP) of 80 mmHg, until the bleeding is surgically controlled [8]. Higher blood pressures (SBP >100 mmHg, mean arterial pressure [MAP] >70 mmHg) are generally sought in head-injured and pregnant patients. This approach provides satisfactory resuscitation of the trauma patient until surgical control of bleeding is achieved.

F LU I D O P T I O N S Crystalloids There is controversy concerning which IV solutions should be used for resuscitation. During hemorrhage, a compensatory increase in reabsorption of fluid into the capillaries partially restores the intravascular compartment but depletes the interstitial space. To replete the intravascular and interstitial compartments, crystalloid solutions such as isotonic 0.9 percent saline or lactated Ringer’s (LR) solution are traditionally used. Glucose-containing solutions are avoided because hyperglycemia is associated with aggravation of central nervous system injury [9, 10] and increased mortality, especially in trauma patients [11]. In large human interventional studies in both surgical and medical intensive care unit (ICU) settings, intensive insulin therapy guided by specific target glucose levels has been shown to improve in-hospital survival [12–14], with the benefit preserved over a 4-year follow-up [15], to prevent critical illness neuropathy, decrease the need for long-term ventilation, and shorten ICU stay [16]. The most prominent effect has been achieved with glucose levels below 110 mg/dL even despite the increased incidence of hypoglycemia. Paradoxically, the effect was most prominent in nondiabetic patients. The effect seemingly depends more on the strict glucose control than on the

dose of insulin, even though nonhypoglycemic effects of insulin are generally well recognized and might play a role. It should be noted that in observational studies, patients with more severe traumatic brain injury have higher blood glucose levels, that is, hyperglycemia might be a marker of injury severity and the predictor of the outcome rather than the causative agent. Improved outcome with strict glucose control might then be due to effects of insulin infusion rather than lowering the glucose level. Some animal studies have suggested that hyperglycemia induced by rapid glucose infusion does not worsen different markers of neurologic injury, survival, and neurologic sequelae of head trauma [17–19]. Other studies refute these results and find euglycemia protective regardless of the insulin dose used [20]. In any case, the routine use of glucose-containing solutions is not justified, and hyperglycemia is treated with insulin. There are not enough clinical data to compare outcomes with 0.9 percent saline versus LR in trauma. LR is mildly hypotonic with respect to plasma and may theoretically be detrimental if given in large volumes to patients with head injury (Table 6.3). Because LR contains 3 mEq/L of calcium, it has been traditionally contraindicated for coinfusion with or dilution of packed red blood cells (pRBCs). This view has been challenged by several authors [21, 22]. It has been shown that dilution of RBCs with LR in a ratio up to 2:1 (RBC to LR) with subsequent incubation at 37◦ C for up to two hours does not lead to clot formation [22], and dilution of RBCs to hematocrit of 35 percent does not slow down the passage of blood through the standard 170-μm filter [21]. Hepatic conversion of lactate to bicarbonate should increase the blood buffering capacity whereas large volumes of 0.9 percent saline (>30 mL/kg) lead to hyperchloremic acidosis [23]. The same concepts hold true when comparing hetastarch diluted in 0.9 percent saline (Hespan) with balanced crystalloid solution-based hetastarch (Hextend) [24, 25]. Hyperchloremic metabolic acidosis is produced because high-chloride solutions displace serum bicarbonate in the extracellular volume. Unlike lactic acidosis, patients with hyperchloremic metabolic acidosis have a normal anion gap and elevated serum chloride. The effects of crystalloid solutions on the coagulation system are complex. With hemodilution up to 20–40 percent, crystalloids produce a hypercoagulable state due to dilution of anticoagulant factors such as antithrombin and by platelet activation [26–28]. After 60 percent hemodilution, both crystalloids and colloids produce a hypocoagulable state [29]. However, animal studies point to attenuation of hypercoagulability and increased blood loss in uncontrolled hemorrhagic shock treated with 0.9 percent saline as opposed to LR [30]. A

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Table 6.3: Asanguinous Fluid Options for Trauma Lactated Ringer’s (LR)

Preferred isotonic crystalloid solution for most trauma resuscitations. Do not mix with blood or use in blood lines because contains calcium.

0.9% saline

Preferred isotonic crystalloid solution for head trauma. Only solution used in blood transfusion lines and to dilute pRBCs. May cause hyperchloremic metabolic acidosis (with normal anion gap) due to excess chloride displacing serum HCO3 .

Hespan (6% hetastarch in 0.9% saline)

High MW hetastarch. Not recommended because of adverse effects on hemostasis, half-life 30 hours. Abandoned at author’s institution in favor of Hextend.

Hextend (6% hetastarch in balanced electrolyte solution)

High MW hetastarch, half-life 30 hours. Less coagulopathy + platelet dysfunction compared with Hespan. Maximum dose 10–15 mL/kg.

Low + medium MW hetastarch

Colloid solutions with less coagulopathy + platelet dysfunction compared with high MW hetastarch. Low MW hetastarch associated with improved muscle oxygen tension, lower markers of inflammation + endothelial activation compared with LR. Available in Europe and Canada. Not currently available in USA.

Albumin (5%)

Little effect on coagulation. May pass into interstitial compartment if impaired vascular integrity with resultant endothelial swelling + impaired microcirculatory perfusion. Increased mortality after head trauma in SAFE study (vs 0.9% saline) [46].

Dextrans and gelatins

Colloid solutions largely abandoned in USA because of negative effects on coagulation + potential for anaphylaxis + hypersensitivity reactions

Hypertonic saline

Variety of solutions/concentrations. May be combined with colloid to prolong duration of action. Efficiently restores intravascular volume + decreases extravascular volume + tissue edema. Decreases ICP + increases CPP. Especially advantageous in prehospital situations + in head trauma with refractory increased ICP. Not associated with improved neurologic outcomes.

MW, molecular weight; ICP, intracranial pressure; CPP, cerebral perfusion pressure, pRBC, packed red blood cells.

head-to-head comparison of these two crystalloid solutions in patients undergoing abdominal aortic aneurysm repair found an increased need for bicarbonate, platelets, and blood products in patients receiving 0.9 percent saline compared with LR. There was no difference in outcomes [31]. In major abdominal surgery, there was no difference in coagulation parameters in patients receiving 0.9 percent saline or LR [32]. At MetroHealth Medical Center, 0.9 percent saline is used primarily in head trauma patients and for co-infusion with blood products; LR is used for most other purposes. Colloids versus Crystalloids The choice of crystalloid or colloid solutions for resuscitation of trauma patients requiring surgery is unresolved (Table 6.3). Factors influencing choice of asanguinous fluids include effects on coagulation, metabolic state, alterations in macro- and microcirculation, volume distribution, and organ function (e.g., kidney function and splanchnic perfusion) [33, 34]. Historically, the crystalloid/colloid controversy has been focused primarily on outcome. There is increasing evidence that mortality is not the correct measure when assessing the ideal volume replacement strategy. Rather, measures such as organ perfusion, organ function, degree of inflammation, immunologic aspects, and wound healing may be more appropriate [35]. Colloid solutions are more effective plasma expanders than crystalloids. They increase the plasma oncotic pressure, which

serves to retain water in the intravascular compartment and minimize interstitial edema in vital organs such as the lung, heart, and brain. Intraoperative use of colloid solutions has been associated with improved outcome and decreased hospital stay [36, 37], possibly because of decreased tissue edema, nausea, vomiting, and pain. Hextend (6% hydroxyethyl starch in a physiologically balanced medium of electrolytes, glucose, and lactate) has a median serum half-life of more than 30 hours [38]. Thus, less overall fluid volume is required and less peripheral edema is produced for the same degree of intravascular volume expansion. Hextend may be beneficial after head injury. For example, in a model of severe traumatic brain injury in pigs, Hextend, used as the sole resuscitation fluid, prevented an increase in intracranial pressure (ICP) and maintained cerebral perfusion pressure (CPP) similar to LR combined with mannitol, while the brain tissue pO2 and neurologic outcomes were significantly better; [39] when compared with the crystalloid plus mannitol standard of care, total fluid requirements were reduced and no adverse effect on the coagulation profile was observed. Compared with 0.9 percent saline, volume resuscitation with Hextend was associated with less metabolic acidosis and longer survival in an animal model of septic shock [40]. Most colloids produce coagulopathy at relatively lower degrees of hemodilution compared with crystalloids [27–29]. Colloids also prevent, to a variable degree, naturally occurring

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platelet activation and hypercoagulability. Hespan (6% hetastarch in 0.9% sodium chloride) has been shown to have adverse effects on hemostasis that include impaired platelet aggregation, type I von Willebrand-like syndrome with decreased factor VIII coagulant activity, decreased von Willebrand factor antigen, and factor VIII-related ristocitin cofactor [41, 42]. This colloid was withdrawn from our hospital formulary and replaced with Hextend, which is associated, both in vitro [43] and in vivo [44], with better thromboelastographic parameters of dynamic clot formation. Hextend does not inhibit platelet function, which may be because its solvent contains 2.5 mmol/L calcium chloride dihydrate [45]. In a randomized, double-blind study on intraoperative fluid replacement, LR produced hypercoagulability, Hespan produced a hypocoagulable state, and Hextend had the least effect on thromboelastographic profile [44]. In a randomized, double-blind trial comparing fluid resuscitation with albumin or 0.9 percent saline on mortality in 6,997 ICU patients, use of either solution resulted in similar outcomes at 28 days. The relative risk of death, proportion of patients with new single-organ and multiple-organ failure, days spent in the ICU, days spent in the hospital, days of mechanical ventilation, and days of renal-replacement therapy were similar between groups [46]. There was, however, increased mortality in headinjured patients randomized to the albumin (59 of 241 patients, 25%) as compared with the saline group (38 of 251 patients, 15%). The effects of colloids versus crystalloids on tissue oxygen tension have been studied [47]. In patients scheduled for major abdominal surgery, volume replacement with low-molecularweight hetastarch (mean molecular weight, 130 kDa; degree of substitution, 0.4), as compared with LR, has resulted in significantly improved muscle oxygen tension, possibly due to reduced endothelial swelling and improved microcirculation. The difference between the groups was apparent despite similar hemodynamics and oxygenation profile and was progressively increasing during the surgery and through the morning of the next day. The influence of different volume replacement regimens on inflammation and endothelial activation in elderly patients undergoing major abdominal surgery was assessed [48]. Patients were randomized to receive LR, 0.9 percent saline, or low-molecular-weight hetastarch 130/0.4. Fluids were given to keep central venous pressure between 8 and 12 mmHg. Although hemodynamics was similar in all groups, markers of inflammation and endothelial injury and activation were significantly higher after crystalloid than after hetastarch 130/0.4 based volume replacement. Resuscitation with crystalloid fluids alone may reduce the plasma oncotic pressure, promote water shift from intravascular to interstitial space, and result in tissue edema [49]. It has been suggested that decreased colloid oncotic pressure from infusion of crystalloid solutions would result in adverse pulmonary outcomes because of interstitial pulmonary edema. In a retrospective study of 512 trauma patients requiring surgery within 24 hours of admission to a Level 1 trauma center, it was shown that, compared with Hextend, resuscitation with crystalloid fluids was not associated with increased duration of mechanical ventilation or worsened alveolar-to-arterial oxygen gradient or oxygen index after surgery. The low mortality rate in both groups supported the effectiveness of both

fluid management strategies in maintaining tissue homeostasis [50]. A meta-analysis failed to detect any differences in survival between crystalloid and colloid resuscitation overall, although it is recognized that many studies on specific solutions have been underpowered [51]. Further, pooling old-to-very old underpowered studies in a meta-analysis is of limited value [52]. Hetastarch accumulates in the body. Because preparations of hetastarch are actually a mixture of complex molecules of different size and structure, only an average half-life of the particular mix can be calculated. Hetastarch is slowly metabolized by intravascular α-amylase. For example, median serum halflife of Hextend is about 30 hours. The smaller hydroxyethyl starch molecules are rapidly eliminated by glomerular filtration. Hemodilution is observed for 24–48 hours after shortterm infusion. A varying amount of hetastarch is taken up by the reticuloendothelial system. Pruritus has been reported after hetastarch infusion [53]. Life-threatening anaphylactic reactions may occur with different kinds of hydroxyethyl starch preparations but appear to be rare [54–56]. A dose limitation exists for all hetastarch preparations ranging from 20 mL/kg (10% hetastarch, 200/0.5) to 50 mL/kg (6% hetastarch, 130/0.4). Different Colloid Formulations The crystalloid/colloid debate has been enlarged to a colloid/colloid debate because several preparations exist, including albumin, dextrans, gelatins, and hetastarch solutions (Table 6.3). Due to their varying physicochemical properties, these solutions widely differ with regard to their pharmacokinetic and pharmacodynamic properties, as well as their hemodynamic efficacy and side effects. Hetastarch is the most intensively studied plasma substitute. The different hetastarch preparations are defined by concentration, molar substitution, mean molecular weight, and the C2/C6 ratio of substitution [35]. In particular, mediummolecular-weight hetastarch with lower molar substitution appears promising compared with first-generation hetastarches [57]. Several hetastarch solutions are available in Europe. In the United States, only the first-generation high-molecularweight 6 percent hetastarch with a high molar substitution (Hespan and Hextend, mean molecular weight, 450 kDa) are approved. In Canada, a medium-molecular-weight 10 percent hetastarch (Pentastarch, mean molecular weight, 270 kDa) is available. In addition to the starch average molecular weight, the weight distribution, degree, and pattern of substitution all can influence the effect on the coagulation [58]. In general, smaller molecule-sized starches, as opposed to the larger ones, and starches diluted in balanced salt solutions, as opposed to 0.9 percent saline, produce less coagulopathy and platelet dysfunction [29]. However, at least in some studies, no clinically relevant differences have been observed [59]. Large amounts of high-molecular-weight 6 percent hetastarch (>15–20 mL/kg) are traditionally avoided because of the well-documented risk of coagulopathy [60], increased blood loss and transfusion requirements [61, 62], and mortality [61, 63]. These effects are mediated by dose-dependent decreases in factor VIII and the von Willebrand factor, and inactivation of GP IIb-IIIa [62]. Hextend, approved for use in the United States

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in 1999, appears to be different from Hespan in its effects on hemostasis [44, 45]. Hextend is the first reported hydroxyethyl starch solution that increases platelet reactivity. It is not clear if this effect is explained completely by the calcium-containing solvent [45, 64]. Albumin is derived from pooled human plasma, heated, and sterilized by ultrafiltration. Its molecular weight is approximately 69 kDa. Albumin is generally accepted to be safe in terms of transmission of infectious diseases with little effect on coagulation. Albumin may have some additional specific effects aside from its volume-replacing properties such as transport function for various drugs and endogenous substances or effects on membrane permeability secondary to free radical scavenging [65, 66]. In patients with impaired vascular endothelial integrity, albumin may pass into the interstitial compartment with resultant endothelial swelling and impaired microcirculatory perfusion [67–69]. Dextrans have been largely abandoned for fluid resuscitation because of the negative effects on coagulation and high anaphylactic potential. Similarly, gelatins were abandoned in the United States because of the high incidence of hypersensitivity reactions. Hypertonic Fluids Use of hypertonic solutions for different populations of critically ill patients has been investigated for more than two decades. The obvious rationale is that a minimal volume of hypertonic saline will draw intracellular water into the extracellular space. Not surprisingly, volume expansion with hypertonic saline is both more efficient and better sustained than with normosmolar fluids. In comparison of the peak hemodilution in healthy volunteers, 7.5 percent saline and 7.5 percent saline in 6 percent dextran were 4.4 and 6.2 times more effective than similar volumes of 0.9 percent saline, respectively. Area under the hemodilution-time curve was 7 times larger for 7.5 percent saline in dextran and 3.8 times larger for 7.5 percent saline than for 0.9 percent saline [70]. As expected, addition of colloid to the hypertonic saline increased the magnitude and markedly prolonged the duration of volume expansion [70, 71]. When a 30-minute infusion of 4 mL/kg of 7.5 percent saline in 6 percent dextran was compared with 25 mL/kg of LR, the peak volume expansion was similar – about 7 mL/kg. However, 30 minutes later, the volume expansion with hypertonic saline-dextran was three times higher than with LR (5.1 ± 0.9 vs. 1.7 ± 0.6 mL/kg). At two hours, for each milliliter of the fluid infused, the remaining intravascular volume expansion was 0.07 mL for LR and 0.7 mL for hypertonic saline-dextran [72]. Hypertonic fluids are especially advantageous in military trauma and other situations (e.g., prehospital, helicopter) when the weight/benefit ratio is crucial. In hemorrhagic shock or local ischemia cells swell [73], absorb water, chloride, and sodium, and lose the resting membrane potential [74]. They return to normal volume, electrolyte balance, and resting potential with hypertonic saline better than with isotonic resuscitation [74]. Capillary lumens narrow as a result of this swelling [75] and return to normal diameter with hypertonic resuscitation but not with LR [76]. Further, hypertonic saline restores intravascular volume and hemodynamics while decreasing extravascular volume and tissue edema [72]. With LR, extravascular volume increased by 60 percent of the

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infused volume at the end of the infusion and by 43 percent at two hours, but with hypertonic saline-dextran, extravascular water decreased by 170 percent and 430 percent of the infused volume, respectively. In brain injury associated with pulmonary edema, hypertonic saline depletes tissue water content better than mannitol [77]. This feature may be crucial in situations such as head trauma (see Chapter 12). Prehospital infusion of 250 mL of 7.5 percent saline with or without dextran, followed by a usual fluid resuscitation, to hypotensive trauma patients was compared with LR [78]. The bolus of hypertonic fluid resulted in improved blood pressure, decreased fluid requirements, and increased survival to discharge, especially in patients with Glasgow Coma Scale less than 8. The rise in the circulating blood volume and cardiac output is immediate [79], although a transient decrease in blood pressure due to vasodilatation may occur [80, 81]. Hypertonic solutions increase cardiac contractility, venous return, and coronary blood flow [81, 82]. Moreover, hypertonic saline/dextran solution is effective in treating dehydration [83] and massive hemorrhage [84] in animals with preexisting dehydration. Hypertonic solutions used in clinical studies vary. The most common regimen is 100–250 mL or 1.5–2 mL/kg of 7.2–7.5 percent saline with or without colloid. The U.S. military recommends a 7.5 percent saline; in Europe, 7.5 percent saline in 6 percent dextran 70 is used. Other regimens include single boluses of 30 mL of 23.4 percent saline, 75 mL of 10 percent saline, or continuous infusions of 3 percent saline. For most studies of head trauma, regardless of the concentration used, the dose of sodium chloride infused with a single fluid bolus in adult patients ranges from approximately 7 to 15 g, or 120 to 300 mEq. Accordingly, results are fairly uniform. A single infusion of hypertonic saline will decrease intracranial pressure by about 70 percent or 10–25 mmHg and increase the cerebral perfusion pressure by 10–30 mmHg; both effects are evident in a matter of minutes, reaching maximum effect by 20–60 minutes, and lasting for 1.5–4 hours, sometimes longer [85–87]. Similar effects have been observed in patients with stroke [88] and subarachnoid hemorrhage [89]. Effects of hypertonic saline on intracranial and cerebral perfusion pressure were more rapid [86] and more profound than a comparable [90] or double [86] volume of 20 percent mannitol, and lasted longer [86, 91]. In a study on trauma patients whose elevated intracranial pressure was refractory to all other modalities [90], 2 mL/kg of hypertonic saline was compared with a similar volume of 20 percent mannitol. In the hypertonic saline group, the number of episodes of elevated intracranial pressure was reduced by almost a half and their cumulative duration by about a third as compared with patients treated with mannitol. Similarly, patients in the hypertonic saline group required 50 percent less volume of cerebrospinal fluid drainage to maintain target intracranial and cerebral perfusion pressure, and the success rate in achieving these targets was 90 percent in the hypertonic saline group versus only 30 percent in the mannitol group. The clinical outcome at 90 days was similar in both groups, however. In a striking study on pediatric head-injured patients whose elevated intracranial pressure had been refractory to all other modalities including mannitol and barbiturate coma [92], continuous infusion of 3 percent saline for the mean of 7.6 days (range, 4–18 days) led to a rapid and sustained improvement in intracranial and cerebral perfusion pressure. The treatment was surprisingly well tolerated, even though on average the serum

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sodium was 171 mEq/L (range, 157–187 mEq/L) and serum osmolality was 365 mOsm/L (range, 330–431 mOsm/L). A cohort study in patients with traumatic brain injury and hypotension compared 7.5 percent saline/6 percent dextran 70 with conventional crystalloid fluid treatment [93]. With the hypertonic fluid, there was a trend for improved survival to discharge in all the subgroups (odds ratios, 1.6–1.8). For patients with initial Glasgow Coma Scale less than 8, the odds ratio for survival until discharge was 2.12 with hypertonic salinedextran versus conventional treatment. On the other hand, in a randomized controlled trial of patients with traumatic brain injury who were comatose (Glasgow Coma Scale score, 35 mmHg

Mixed venous oxygen saturation (central venous or pulmonary artery)

>65%

Base deficit

2 hours). Invasive measurement of ICP may be appropriate in those patients with only mild to moderate TBI. Intracranial hematomas and cerebral edema may appear or worsen after the initial CT scan for up to 48 hours after the injury; frequent neurologic examinations or continuous ICP monitoring seems particularly justified in this time period [55, 56]. Cases should be individualized and discussed with the neurosurgical service prior to surgery. There are different techniques for monitoring ICP (see Figure 11.5). The gold standard is an intraventricular catheter. As this catheter is connected to an external pressure transducer, it can be recalibrated as necessary to maintain its accuracy. In addition, it allows therapeutic intervention for intracranial hypertension through drainage of CSF. Its main disadvantage is an increased risk of infection. Another commonly used monitor is a fiberoptic catheter placed in the brain parenchyma. This system is relatively easy to insert and is associated with fewer complications. Whereas the ventricular catheter with the external pressure transducer can be recalibrated as necessary, the parenchymal ICP monitor is calibrated prior to insertion without the possibility of further recalibration. As a result, drift impairs the accuracy of this type of monitor over time. Other types of ICP monitors include epidural systems and subarachnoid bolts. These monitors are thought to be less accurate than the ventricular catheter and the parenchymal fiberoptic monitor, and are used infrequently. The normal upper limit of ICP is 10–15 mmHg and most authorities recommend treatment when the ICP exceeds 20– 25 mmHg. Specific therapies to decrease ICP will be discussed later. The ICP tracing has normal variability over the course

Figure 11.5. Different modalities to monitor intracranial pressure.

of the cardiac cycle. Prolonged elevation in ICP is pathologic, however. One type of ICP elevation, termed the A wave or delta wave, deserves special consideration. Originally described by Lundberg and then studied by Rosner and Becker, this wave is a large increase in ICP to 60–80 mmHg lasting 5 to 20 minutes [57, 58]. It usually portends an ominous outcome. The inciting event is a drop in CPP that causes the autoregulatory mechanism to induce cerebral vasodilation. This response increases cerebral blood volume and ICP, and thus further compromises CPP. Treatment of A waves includes improving intracranial compliance, increasing CPP, and avoiding stimuli that either increase ICP or lower blood pressure. Jugular Venous Oxygenation A jugular venous bulb catheter with continuous oximetry measures the saturation of the venous drainage from the brain (SjvO2 ). Inadequate perfusion increases the oxygen extraction ratio in the brain and causes a drop in SjvO2 . On the other hand, a non-functioning brain extracting little oxygen will result in a high SjvO2 value. An SjvO2 below 50 percent or higher than 75 percent has been associated with poor prognosis [59, 60]. Such catheters are particularly useful in TBI when a measure such as hyperventilation, which reduces global CBF without reducing cerebral metabolic rate, is used. In addition, lactate levels on blood samples drawn from this catheter can reveal anaerobic metabolism in the brain if they show a higher lactate level than that in arterial blood drawn simultaneously. The limitation of the jugular bulb catheter is that it only offers insight into the global balance of cerebral blood flow and metabolism. SjvO2 values can be in the normal range despite small regional areas of ongoing ischemia. Brain Tissue Oxygenation Some intraparenchymal catheters may combine ICP monitoring with a miniature Clark-type electrode to measure brain tissue oxygenation (tPO2 ). This monitor provides a continuous measurement of oxygen tension in the brain parenchyma, which reflects the local balance between supply and demand

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of oxygen. Doppenberg et al. [61] showed a close correlation between tPO2 and CBF, finding that a tPO2 of 26 mmHg was approximately equivalent to a CBF at the ischemic threshold of 18 mL/100 g/min. Zauner et al. [62] showed that tPO2 of approximately 39 mmHg correlated with a good outcome and 19 mmHg with a bad outcome, offering some guidance for therapeutic interventions. The best method for intervening for a low tPO2 has not been established, however. Presumably any intervention that increases CBF, decreases CMRO2 , or increases the oxygen content of blood would improve tPO2 . Such interventions include raising CPP, using sedative drugs to suppress CMRO2 , or raising hematocrit. Due to the limited amount of oxygen that is dissolved in the blood apart from hemoglobin, increasing the PaO2 alone would not be expected to raise tPO2 . Paradoxically, increasing FiO2 frequently does raise tPO2 , and is often deployed, even when the saturation of hemoglobin is already at or near 100 percent. This effect is difficult to explain, and adds uncertainty to the value of this monitor .

M A N AG E M E N T P R I N C I P L E S Intracranial Pressure and Cerebral Perfusion Pressure (ICP/CPP) Intracranial hypertension predisposes patients to poor outcomes [63–65]. The main goal for patients with TBI is to control ICP and provide an appropriate CPP, defined as MAP – ICP; many techniques are available to shift this balance in a favorable direction (see Table 11.5). Some controversy exists regarding what constitutes the optimal ICP and CPP. Prior recommendations were to maintain the CPP at 70 mmHg or above and to lower ICP when it exceeded 20–25 mmHg [66, 67]. Subsequently CPP goals were redefined to be kept between 60 mmHg and 70 mmHg, as aggressive attempts to raise CPP beyond 70 mmHg increase the incidence of ARDS [46, 68]. Another recent source recommends a CPP of 50 mmHg [1].

Table 11.5: Methods for Controlling Intracranial Pressure Cerebrospinal fluid (CSF)

Brain

Blood volume

Mannitol or other hypertonic solution External CSF drainage ■ Ventricular catheter ■ Lumbar drain ■ VP or VA shunt ■ Serial lumbar punctures Mannitol or hypertonic saline ± furosemide Decompressive craniectomy Resection of contusion or other mass lesion

Osmotic Therapy Reduction of ICP in patients with head injuries can be accomplished effectively by using osmotic diuretics. Mannitol is the most commonly used agent and is available for intravenous administration in either a 20 or 25 percent solution. Common dosages range from 0.25 to 1 g/kg of body weight. Mannitol may be used on a repeated schedule, but the serum osmolarity must be monitored to ensure that systemic dehydration, which can be particularly injurious to the kidneys, does not take place. Serum osmolarity should not be allowed to exceed 320 mOsm. The mechanism of ICP reduction by mannitol may be related to its osmotic effect in shifting fluid from the brain tissue compartment to the intravascular compartment as well as its ability to improve blood rheology by decreasing blood viscosity [69, 70]. The latter effect has been postulated to cause reflex vasoconstriction, which keeps blood flow constant while reducing blood volume and ICP. In addition, mannitol, like other hypertonic fluids, decreases production of cerebrospinal fluid (CSF). Some individuals may benefit from the use of furosemide in combination with mannitol. The duration of the ICP decrease due to the two diuretics together may be prolonged over either agent used alone [71]. Various concentrations of hypertonic saline alone or in combination with dextran have been used for management of elevated ICP, primarily in the setting of intracranial hypertension refractory to mannitol therapy. As the blood–brain barrier is impermeable to sodium ions, hypertonic saline establishes a gradient that facilitates the movement of water from the brain into the intravascular space. Evidence indicates that hypertonic saline may be more effective in controlling ICP than mannitol [72]. In addition to efficacy, the proposed benefit of hypertonic saline is lack of severe electrolyte disturbance, which is common with mannitol. The brisk diuresis seen with mannitol is absent with hypertonic saline. Although hypertonic saline has been administered both as a bolus and as a continuous infusion, currently no firm guidelines have been established for its use. In addition, no standard concentration has been established for clinical use, although most clinical studies have used either 7.5 percent or 3 percent in an infusion at a rate of 20–40 mL/h. Following prolonged infusion in the intensive care unit, hypertonic saline should be tapered off slowly to prevent subsequent hyponatremia and rebound edema. Hypertonic saline should only be administered through a central line. In situations where hypertonic saline causes an unacceptable hyperchloremic acidosis, a mixture of sodium chloride and sodium acetate can be used.

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Ventilation

Mannitol Hyperventilation Hypothermia Head elevation, neutral neck position Deep propofol or barbiturate sedation ■ ± paralysis Control of seizures

Hyperventilation is an effective way to reduce ICP. It is useful in the setting of an acutely increased ICP that needs to be controlled until more definitive therapy can be initiated. Hyperventilation may be useful in the initial stages of resuscitation of head-injured patients or in a patient who suddenly develops signs of herniation. Hyperventilation causes cerebral vasoconstriction, primarily in the small regulatory arteries in the brain; this vasoconstriction reduces the cerebral blood volume and therefore the ICP. The decrease in cerebral blood volume and the fall in ICP occur virtually simultaneously with initiation of hyperventilation. The reduction in cerebral blood volume is achieved at the expense of CBF, however.

VP, ventriculoperitoneal shunt; VA, ventriculoatrial shunt.

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The use of hyperventilation in patients with brain injury is fraught with controversy: the degree of hyperventilation that should be employed is unknown, and the duration of hyperventilation that can be used safely and effectively is uncertain. The overriding concern is that excessive or prolonged hyperventilation may cause cerebral ischemia by decreasing CBF [73]. Current recommendations are that patients who are head injured should be maintained at normocapnia except when hypocapnia is necessary to control acute increases in ICP. Chronic hyperventilation should be avoided if possible. In situations where prolonged hyperventilation is necessary because of failure of other agents to control ICP, monitoring tPO2 , SjvO2 , and cerebral venous lactate are desirable to avoid hypocapnia-induced ischemia [74]. Coagulopathy The brain is rich in tissue thromboplastin, and severe TBI with contusion can lead to consumption coagulopathy and/or disseminated intravascular coagulopathy [75]. The presence of coagulopathy in TBI is an indicator of poor prognosis [76]. When observed clinically, it must be treated vigorously as guided by the coagulation profile. Fresh-frozen plasma is indicated when the International Normalized Ratio (INR) exceeds 1.4, and platelets should be given when the count is below 100,000. Platelets should also be given if the patient is receiving aspirin therapy and there is clinical bleeding despite a normal platelet count. An increasing number of elderly patients admitted with TBI from falls are on coumadin for atrial fibrillation or prevention of stroke. These can be very difficult cases because there is often insufficient time to correct coagulopathy before bringing the patient to the operating room. Activated recombinant Factor VII may be useful as an immediate therapeutic measure under these circumstances. Despite its theoretical benefits, systemic hypothermia can aggravate coagulopathy, the presence of which should prompt aggressive warming of the patient (see Chapter 29). Glycemic Control The development of hyperglycemia in patients with severe TBI is associated with poor prognosis [77, 78]. Although this may be partly related to the stress response to trauma, substantial clinical and experimental evidence suggest that control of hyperglycemia may improve outcome [79]. As demonstrated in other critically ill patients, tight hyperglycemic control is achieved at the risk of hypoglycemia, which is detrimental to the brain. Not only is glucose the main fuel substrate for the brain, there is evidence that patients with severe brain trauma may develop hyperglycolysis [80]. Thus, it is prudent to treat hyperglycemia in patients with TBI, but caution must be exercised and a reasonable goal would be 140 mg/dl. Electrolyte Disturbance Patients with severe TBI or other brain injury can develop diabetes insipidus or syndrome of inappropriate antidiuretic hormone. The former usually leads to hypernatremia, whereas the latter results in hyponatremia. Determination of plasma and urine sodium as well as osmolality generally will sort out the diagnosis, allowing institution of appropriate treatment.

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Crystalloid versus Colloid When the blood–brain barrier is intact, movement of water in and out of the brain is essentially governed by the osmotic gradient, and oncotic pressure has little influence. When the blood–brain barrier is partially disrupted, colloid may have a theoretical advantage, as has been demonstrated in experimental cerebral ischemia. However, there is no clinical evidence to support the use of colloids in TBI. In a clinical trial comparing colloid vs. crystalloid as a resuscitation fluid in critically ill patients, no difference could be demonstrated [81] (see also Chapter 6). Moreover, in a subgroup analysis of patients with brain trauma, the mortality rate was significantly higher in the 4 percent albumin group than the saline group. Another commonly used colloid, hydroxyethyl starch, can aggravate coagulopathy, even in small doses, and should be avoided in patients with brain injuries [82]. Thus, hypertonic or isotonic crystalloid is the preferred fluid in patients with TBI, and the most appropriate colloid to be used is blood when indicated. Otherwise, albumin is preferable to hydroxyethyl starch. Regarding blood transfusion, no current guideline exists on the threshold in patients with TBI. Although a restrictive strategy (hematocrit of 21 percent) is associated with better outcome in critically ill patients, patients with TBI have not been specifically studied. Monitors including jugular venous oximetry and brain tissue oxygen tension may help the decision-making process regarding blood transfusion. As a general principle, if ongoing cerebral ischemia is suspected, it may be prudent to maintain a higher hematocrit, for example, 27 to 30 percent. Hypothermia Moderate hypothermia has been considered as a therapeutic modality in head injury for many years. The theoretical benefits of hypothermia in preventing secondary brain injury may be related to its effects on attenuating the biochemical cascade that begins at the time of injury or on controlling intracranial hypertension. Despite these actions, a large multicenter clinical trial of head-injured patients demonstrated no benefit to the induction of hypothermia [83]. A post hoc analysis of the data from this study did show that head-injured patients younger than 45 years who were mildly hypothermic (less than 35◦ C) on admission had a lower incidence of poor outcome if they were randomly assigned to the hypothermia arm [84]. It was not clear, however, whether the benefit seen in this group of patients is actually from early hypothermia or from avoidance of the rewarming process. Given the rather limited situation in which hypothermia appears to be beneficial in head injury, it is not recommended for routine use [85]. In addition, hypothermia increases the risk of pneumonia and wound infection and may cause electrolyte and coagulation abnormalities [86] (see Chapter 29). Because of the theoretical benefits and consistent evidence of cerebral protection in experimental ischemia, an extension of the original hypothermia trial examining the subset of patients who were admitted cold, as well as a pediatric head trauma trial, is ongoing [87]. Hypothermia does decrease ICP, however, primarily because it decreases cerebral metabolic rate and thus CBF. Despite the controversies surrounding the use of hypothermia in head injury, hypothermia is useful in the setting of intracranial hypertension refractory to other interventions and may improve outcome [88].

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In contrast to hypothermia, the devastating effects of hyperthermia are well established, and fever in a brain-injured patient must be treated promptly and vigorously. Pharmacology Barbiturates may be used as an adjunct to other therapy for controlling ICP. Given that CBF is coupled to cerebral metabolism, the effect of barbiturates on ICP is thought to be due to a decrease in cerebral metabolic rate, which leads to a decrease in CBF, cerebral blood volume, and thus ICP. As long as the MAP is maintained, CPP will improve. In addition, barbiturates may have an antioxidant effect, thus limiting the secondary injury from free radicals. Barbiturate therapy is appropriate only in patients who are hemodynamically stable and have been adequately resuscitated. It should not be employed if MAP and CPP cannot be appropriately maintained. Some patients with refractory elevations in ICP have sustained extensive neurologic injury, and their cerebral metabolic rate may already be low; failure to respond to barbiturates carries with it an ominous prognosis [67]. In addition, the use of barbiturate coma is associated with immunologic suppression with increased risk of pneumonia and sepsis. Propofol may function in a similar manner to barbiturates by decreasing cerebral metabolic rate, cerebral blood volume, and ICP. It has the same hemodynamic risks as barbiturates and has the additional risk of causing a metabolic acidosis and myocardial dysfunction with prolonged infusions. This propofol infusion syndrome carries significant morbidity and mortality [89, 90]. Both barbiturates and propofol can be used in a dose– response manner to provide ICP control, ranging from mild sedation to pharmacologically induced coma. Although some type of electroencephalography (EEG), such as a bispectral index, has been advocated for sedation, it is not necessary at low-dose infusion. Continuous EEG monitoring must be employed, however, when either propofol or a barbiturate is used to achieve maximal suppression of metabolic activity. The infusion is titrated against the EEG activity, with the goal of achieving burst suppression. Although any barbiturate could be given to achieve burst suppression, pentobarbital is most commonly used in the ICU and thiopental is most common in the operating room (OR). Titration of the infusion against EEG burst suppression is an effective means to achieve maximal reduction in CMRO2 . Use of Steroids Steroids have profound anti-inflammatory actions and can reduce brain edema. They have been used for brain trauma in the past without evidence for their benefits. Although marginal, the purported benefits of high-dose methylprednisolone treatment in spinal cord injury have prompted revived interest in the use of steroids in TBI. However, results from the CRASH trial indicated that, not only does steroid use show no benefit in TBI, it quite possibly increases mortality and morbidity because of increased incidence of pneumonia and infection [91]. Decompressive Craniectomy Decompressive craniectomy has been used in the past to manage intractable intracranial hypertension after TBI. The rationale

for its use is based on the Monro–Kellie Doctrine, which states that the intracranial compartment is a fixed space and can only accommodate a very small volume (translocation of CSF to the spinal axis) before pressure increases. Therefore, in patients who have sustained a TBI and have severe cerebral edema, it postulated that removing a large portion of the skull will allow more room for the increased volume of brain and thus decrease intracranial pressure [92, 93]. Decompressive craniectomy has also been shown to improve brain tissue oxygenation [94, 95]. However, the question that remains is whether this intervention improves outcome. As well, potential complications with this procedure include increased cerebral edema and infection [93]. A retrospective cohort study by Aarabi and coworkers reported a 50 percent incidence of good recovery in 50 patients [96]. Definitive answers will hopefully be supplied by RESCUE ICP, a multicenter randomized controlled study that is currently enrolling patients (www.rescueicp.com ). A N E S T H E T I C M A N AG E M E N T Patients requiring surgery after sustaining a TBI can be subdivided into two major groups with different perioperative concerns. These groups include those requiring emergent and nonemergent surgery. The emergent group can also be subdivided into neurosurgical procedures and nonneurosurgical procedures. The anesthetic management of these groups will be discussed below Emergent Surgery Neurosurgical These patients commonly arrive in the operating room with an endotracheal tube in place. If they are not tracheally intubated, the same principles that were discussed in the section on airway should be applied. Often there is little time allotted for the preoperative assessment; one’s approach must be concise and focused to obtain the pertinent information in a brief amount of time. These patients will probably have other systemic injuries that need to be assessed and addressed. The neurologic condition of the patient can be determined by obtaining the GCS score, reviewing the CT scan findings, and examining the pupils. Frequently patients with TBI are intoxicated. The presence of alcohol and other psychoactive agents may influence the response of the patient to anesthetic agents. Their anesthetic requirement may be decreased, or increased depending on the substances ingested. In patients with decreased level of consciousness, the risk of aspiration with subsequent pneumonitis is ever present. The hemodynamic status of the patient is also extremely important. Patients may demonstrate Cushing’s response of hypertension and bradycardia, which signifies brainstem compression from raised ICP. However, these classic findings may be masked by hypovolemia, and their absence does not rule out brain stem compression. An assessment of volume status is therefore always indicated. This is often difficult to accomplish as urine output may be increased by the use of mannitol, and hematocrit is decreased by ongoing blood loss. Significant systolic variation during positive ventilation is a positive indicator for hypovolemia (see Chapter 5). In general, a strong index of suspicion should be maintained, and volume challenge of

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500 mL of crystalloid should be given whenever hypovolemia is suspected. In adults, isolated brain injury generally does not result in systemic hypotension, although this can occur in small children with scalp blood loss alone. The presence of hypotension in an adult with an isolated brain injury should prompt reevaluation of all other systems to rule out other sources of blood loss, for example, a ruptured spleen. Other information to obtain includes the status of oxygenation, acid-base balance, electrolytes, hematocrit, coagulation profile including platelet count, and the presence of other injuries. The information obtained above will, in part, determine the most appropriate direction in which to proceed. Appropriate monitoring must be established and must also take into account the immediate need for surgical decompression. Standard monitors include electrocardiography, pulse oximetry, capnography, temperature, urine output, and noninvasive blood pressure measurement. An arterial catheter is highly desirable, for continuous blood pressure monitoring and blood sampling, but its placement should not delay obtaining adequate intravenous access. Two large-bore intravenous catheters are required at a minimum. Although a central venous catheter and retrograde jugular bulb catheter may be of value, time constraints usually do not permit their insertion. These patients usually do not have ICP monitors in place but one can assume the presence of intracranial hypertension in the setting of an acute space-occupying lesion because the brain is unable to accommodate sudden increases in intracranial volume. The presence of midline shift and pupillary abnormalities confirm this diagnosis. Therefore, these patients should be hyperventilated until the dura is opened. Notice this is a different situation than the situation of chronic hyperventilation mentioned previously, which may cause cerebral edema and worsened clinical outcomes [97, 98]. The elevation in ICP is more detrimental than the effects of short-term hyperventilation [99]. Another area to focus on is the management of blood pressure. These patients are often hypertensive. The hypertension is often a compensatory mechanism to maintain adequate perfusion of the brain in the setting of raised intracranial pressure. This hypertension should be tolerated in the period before the cranium has been opened. Hypotension during this period should be treated aggressively. Assuming a minimum ICP of 20 mmHg, mean arterial blood pressure should be at least 80 mmHg. A combination of fluid and vasopressors may be used to accomplish this goal. Intravenous volume loading in the early stages of the anesthetic is appropriate, particularly in patients with other injuries and significant blood loss, as the hypertensive response can mask hypovolemia. When the ICP is relieved surgically, the loss of sympathetic drive can result in sudden profound hypotension if adequate intravascular volume has not been restored. Until adequate volume resuscitation is accomplished, small bolus doses of epinephrine may be necessary. The choice of anesthetic agents should be based on the clinical condition of the patient. As a general rule, nondepolarizing neuromuscular blocking agents should be administered to prevent inadvertent movement or coughing while in Mayfield pins. The general goals of anesthesia are similar to the management goals that have been discussed previously. The most important goals are to prevent increases in ICP and to maintain CPP. Intravenous anesthetics seem well suited for this goal. Both thiopen-

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tal and propofol decrease CMRO2 and subsequently decrease cerebral blood flow due to flow metabolism coupling [37, 100]. These agents have also been shown to decrease ICP in headinjured patients [67, 101]. As well, they may offer some degree of neuroprotection and do not impair flow metabolism coupling or cerebral autoregulation [102–105]. The disadvantage of using thiopental is the prolonged emergence time. However, this problem is not relevant to the majority of patients, as they will be transferred to the ICU, intubated, and sedated for ongoing care. Volatile anesthetic agents may be used as well. Their main advantage is the ease and speed of titration, especially for the newer agents, sevoflurane and desflurane. Similar to the intravenous agents, they may offer neuroprotection [106, 107]. Isoflurane and, to a lesser extent, sevoflurane lead to increases in cerebral blood flow in a dose-dependant manner, and thus may potentially increase ICP [108, 109]. These effects can be minimized by keeping the dose under 1 MAC, but increases in ICP have been reported to occur at these levels [110–112]. In addition, volatile agents may impair cerebral autoregulation although sevoflurane has less of an effect than isoflurane [113]. Consequently, with high or labile ICP, the anesthetic of choice is an intravenous technique with a thiopental or propofol infusion. Care must be taken to avoid overdosage, and the associated hypotension and compromise of CPP. In a retrospective study by Pietropaoli and colleagues, intraoperative hypotension was associated with an increase in mortality and should be avoided [114]. Once the dura is open, decisions on anesthetic management can be based on the appearance of the brain. When an ICP monitor is in place and the ICP is controlled, it is reasonable to choose a volatile agent and switch to either propofol or thiopental should the ICP increase. Nitrous oxide increases CMRO2 , cerebral blood flow, and ICP in head-injured patients and should be avoided [115–117]. Opioids can be used safely in these patients as long as blood pressure is not compromised and the patient is mechanically ventilated. As mentioned earlier, surgical intervention for mass lesions may result in postdecompressive hypotension. This phenomenon was studied retrospectively by Kawaguchi and colleagues who found the major risk factors were low GCS score, absence of basal cisterns on CT, and bilateral dilated pupils [118]. It is better to prevent this event than to treat it. Adequate volume resuscitation prior to dural opening is therefore essential. Continuous monitoring of the arterial blood pressure waveform during mechanical ventilation (systolic pressure variation and pulse pressure variation) may provide important clues to hypovolemia and fluid responsiveness (see Chapter 5). Should hypotension occur, continued volume administration along with vasopressors is appropriate. As discussed previously, there has been a renewed interest in decompressive craniectomy for intractable intracranial hypertension. Although this has not been studied, presumably these patients are also at risk for hypotension on dural opening. Nonneurosurgical Trauma patients who present for emergent surgical management of noncranial injuries, but who also have a concurrent TBI, are complex and can be an anesthetic challenge. These patients are obviously critically ill and at high risk for significant morbidity and mortality. At times, patients must be taken directly to the OR for life-saving procedures prior to undergoing an adequate neurologic examination or head CT.

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In this situation, the main goal is resuscitation and correction of hypotension. The most immediately life-threatening condition must take priority, but the potential presence of the TBI should be kept in mind. Specifically, a history on the level of consciousness should be obtained and the pupils examined. If asymmetry exists or the history suggests a high likelihood of intracranial injury, a consultation with the neurosurgeon should be obtained to initiate ICP monitoring. The presence of dilated pupils bilaterally may suggest brain death or a nonsalvageable patient. This can be confirmed intraoperatively with the use of transcranial Doppler ultrasonography [119]. Transcranial Doppler may also be useful as a semiquantitative noninvasive assessment of ICP if the presence of coagulopathy precludes the placement of an ICP monitor. If the patient is stabilized, surgery can be followed by a CT scan of the head and a possible return to the OR for definitive neurosurgical management. If an ICP monitor is placed and demonstrates intracranial hypertension, management should be as discussed earlier. Nonemergent Patients who have sustained TBI frequently have other injuries, especially fractures requiring operative fixation (see Chapter 15). The timing of surgery in these patients remains a controversial issue [120]. One must balance the need for operative fixation of these fractures to decrease the incidence of complications related to immobility, such as atelectasis, pneumonia, and venous thromboembolism, with the risks of performing surgery in patients with unstable head injuries. These patients have altered physiologic mechanisms such as cerebral autoregulation and are extremely susceptible to secondary brain insults, especially hypotension [26, 115, 121]. The review by Grotz and colleagues summarizes the literature that is replete with retrospective series, some in favor of early fixation and some in favor of delayed fixation [120]. However, none of these studies provides sufficient evidence to guide management of these patients. This can only be accomplished with a prospective randomized trial powered to detect differences in neurologic status as its primary outcome. In the absence of good evidence, the following recommendations provide a conservative approach to management of these patients: (1) Uncontrolled intracranial hypertension should preclude all but emergent surgery; (2) patients with an abnormal head CT scan should have ICP monitoring in the operating room, in particular, for long-duration surgeries in the first 48 hours after injury; (3) consideration should be given to advanced neuromonitoring, including transcranial Doppler, jugular bulb oximetry, and brain tissue oxygenation; and (4) surgery should be terminated and a head CT should be obtained should ICP become unstable. OUTCOME Overall, the outcome of patients with severe TBI has continued to improve over the past 30 years. Most authorities contribute this to improvements in overall trauma care and critical care as opposed to specific interventions [122]. Mortality was 25 percent in a large randomized trial in the mid-1990s, compared with 31 percent in the European Brain Injury Consortium in

the early 1990s, and 44 percent in the Traumatic Coma Data bank in the mid-1980s [123, 124]. Several studies have addressed the prognostication of outcome following TBI. Although there have been slight differences in the study results, most agree the main prognosticators are age, pupillary response, and GCS motor score [125–128]. The 2005 article by Hukkelhoven and colleagues also included hypoxia, hypotension, CT classification, and the presence of traumatic subarachnoid hemorrhage [128].


1. Which of the following is correct with regard to TBI? a. Injury occurring at the scene is termed primary injury. b. Secondary injuries due to hypoxia and hypotension are not preventable. c. Open fractures do not usually require surgery. d. Skull fractures are always associated with intracranial lesions. 2. With regard to primary TBI, which of the following is correct? a. Diffuse axonal injury is best diagnosed using computed tomography (CT). b. Cerebral hematoma may require decompressive craniectomy for refractory intracranial hypertension. c. Epidural hematoma has a worse prognosis compared with intracerebral hematoma. d. Subdural hematoma is the least frequent injury. 3. Considering the initial resuscitation of the patient with TBI, which of the following is correct? a. Cricoid pressure is rarely done for rapid sequence intubation in the field. b. Tracheal intubation should ideally be accomplished via the nasal route. c. Succinylcholine is contraindicated in head injury patients. d. Thiopental may cause severe hypotension in hypovolemic brain injured patients. 4. Concerning fluid and drug administration in hypotensive TBI patients, which of the following is correct? a. Patients should be run dry in order to minimize cerebral edema. b. Hypotonic fluids should be avoided. c. Vasopressors and inotropes should be avoided. d. Mean arterial pressure should be maintained in the 100– 110 mmHg range. 5. Regarding intracranial pressure (ICP) monitoring of the TBI patient, which of the following is correct? a. Cerebral perfusion pressure is not affected by ICP. b. Intraventricular catheters cannot measure ICP accurately. c. The upper limit of normal for ICP is 25 mmHg. d. Intracranial pressure monitoring is recommended for patients with an abnormal head CT and Glasgow Coma Scale score 50% of major muscle groups

ASIA E

Intact

No motor or sensory deficit

blood pressure. Higher cord lesions result in greater sympathectomy, vasodilation, and thus increased vascular capacitance. Although volume is beneficial in this setting, a pure alpha agonist such as phenylephrine is a reasonable choice to restore vascular tone. Patients with higher lesions, in the upper thoracic or cervical spine, with concomitant hypotension and bradycardia are not well served by phenylephrine. Dopamine is a reasonable choice to restore both cardiac inotropy, chronotropy, and peripheral vascular tone. Radiologic Evaluation As part of the secondary survey of the trauma patient, the radiologic evaluation is frequently initiated with anterior-posterior (AP) chest, pelvis, and lateral cervical spine films. In a hemodynamically stable and neurologically intact patient without distracting injuries or recent use of sedatives or opioids following a trauma with minimal mechanism for serious spine injury, the radiologic evaluation of the spine may stop at this point. In fact, patients who meet the above criteria may be able to forego radiologic evaluation of the spine entirely [12]. Clinical evaluation for tenderness to palpation and with movement may be sufficient to clear the spine, but there is some controversy regarding which criteria best select patients who do not need radiographic imaging [13]. Obviously most major trauma patients do not meet these criteria, and further evaluation is necessary. The best approach to imaging of the spine is controversial, however, and dictated by the stability of the patient, the nature of the neurologic deficit, and the extent of other injuries [14]. In addition, with the continued improvement of both the resolution and speed of computed tomography (CT) scans, the role of plain films is likely to diminish over time.

A

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Thorough evaluation of the cervical spine requires AP, lateral, and open-mouth odontoid films. With a tracheally intubated trauma patient, a cervical spine CT may be more practical. In addition, should any abnormality be noted on plain film, a CT scan through the area is essential. Plain films of the thoracic and lumbar spine are indicated in trauma patients who are unexaminable, have definite cervical spine injury or neurologic deficit, have sustained significant trauma to the chest, have injuries that frequently coexist with spine injuries in this region, or have other indications of significant mechanism, such as a seat belt sign [15]. Inadequate plain films should be followed up with a CT scan through the region. Injuries on plain films should also prompt further CT imaging. While CT scans are most sensitive for bony injury, magnetic resonance imaging (MRI) is well suited to detect soft tissue injury, including SCI. The role for MRI in evaluation of the spine in the acute period is currently unclear. Its utility is somewhat limited by the length of time to acquire an image. There are, however, several situations in which it is clearly useful. The presence of a neurologic deficit that is inconsistent with the injury found on plain films and CT should prompt an MRI evaluation. In addition, patients without radiographic evidence of injury who have neurologic deficit may have SCIWORA and should certainly undergo MRI evaluation. SCIWORA, first described by Pang and Wilberger [16] is a type of SCI found in the pediatric population characterized by an absence of bony injury despite the presence of neurologic deficit. The malleability of the pediatric spine allows inappropriate movement of the spinal column with insult to the cord, which may be detected on MRI as cord transection, hemorrhage, or edema [17].

Role for Steroids Methylprednisolone has become a common therapy for patients with neurologic deficit following SCI. Its use was precipitated by the NASCIS (National Spinal Cord Injury Study) II and III studies from the 1990s, which showed clinically important improvement in the motor function of patients with SCI [18–20]. Although these changes in motor function are modest, one to two levels of improvement of motor level can be quite significant if the injury is in the cervical spine. The results of the studies confirming benefit of methylprednisolone have been criticized, [21] however, and some centers do not regard steroids as standard of care. There are numerous reasons why avoidance of systemic steroids might be desirable if they are not indicated, such as their association with hyperglycemia, infection, and polyneuropathy of critical illness. In addition, because the SCI patient population has a high incidence of comorbid head

C

D

Figure 14.7. Several types of spinal cord injuries. (A) Cross-sectional representation of the uninjured spinal cord. (B) Brown–Séquard, with unilateral injury to gray and white matter. (C) Central cord syndrome, with sparing of the tracts near the surface of the cord. (D) Anterior cord syndrome due to disruption of the anterior spinal artery.

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injury, it is worthwhile to consider a large randomized study of methylprednisolone therapy in patients with head injury, which found an increased risk of death in patients receiving methylprednisolone both at two weeks [22] and at six months [23]. If steroids are harmful to the brain, can they really be beneficial to the remainder of the central nervous system in trauma? We have no definitive answer for this question. It is difficult to reconcile the findings of NASCIS with those of CRASH (Corticosteroid Randomization After Significant Head injury), however. In the setting of combined spine and brain injury, is the benefit of steroids sufficient to justify their use? The benefit of methylprednisolone is modest, and its use in someone with concomitant traumatic brain injury is probably inappropriate. Arguments can be made for administering steroids in certain circumstances, however. For example, one might argue that in the setting of a mild traumatic brain injury and a mid-cervical spine injury, the benefit of a modest improvement in motor function, which could mean the difference between long-term ventilator support and the ability to breathe without assistance, the potential benefit outweighs the risk of methylprednisolone. Ultimately the decision to use steroids must be carefully considered on an individual basis by the clinician caring for the patient. Timing of Surgical Intervention The purpose of surgical intervention is to decompress the neural structures and stabilize the spinal column to prevent further injury to the cord. Management of the patient with SCI frequently requires intervention for comorbid life-threatening trauma, such as intraabdominal or pelvic hemorrhage (see Chapters 10 and 15). Surgical decompression of the spinal cord with fixation of the spinal column must wait until the patient is clinically appropriate for the procedure. If the patient remains hemodynamically unstable or develops acute respiratory distress syndrome, then the delay may be significant, from days to weeks. Although there are data to suggest that early operative fixation of isolated SCI decreases the length of stay in the intensive care unit (ICU), [24] improved neurologic outcome has been demonstrated thus far, primarily in animal models, not in humans; [25] early fixation (within 24 hours) is probably most appropriate for cervical spine injuries with tetraplegia [26, 27]. I N T R AO P E R AT I V E M A N AG E M E N T Anesthetic Induction and Airway Management If a patient with SCI did not require endotracheal intubation in the prehospital or emergency department setting, then he or she will need further airway management upon presentation to the operating room (OR). Given the less urgent nature of intubation in this setting, options in addition to the rapid sequence intubation with inline stabilization may be explored by the anesthesiologist. By the time some patients arrive in the OR for surgery, they may have been cleared both radiologically and clinically of cervical spine injury. The technique for induction of anesthesia and endotracheal intubation should therefore be determined by their other injuries, comorbidities, and airway exam. Patients with confirmed cervical spine injury require careful planning, however. These patients will undoubtedly be immo-

bilized in either a cervical collar or Halo device. A rapid sequence induction remains a viable option, particularly in someone who is unable to cooperate with an awake procedure. If the patient has fasted, a standard induction followed by intubation with inline stabilization may be a reasonable option as well. Some consideration should be given to the risk of aspiration, however. Even if sufficient time has passed since the last meal, the stomach may not have emptied adequately for a standard induction. The stress of trauma, narcotics, and ileus due to SCI may all put the patient at risk for aspiration. The most conservative approach to airway management in this setting is the awake fiberoptic oral-endotracheal or nasalendotracheal intubation (see Chapter 2). Glycopyrrolate can be used to decrease secretions and oxymetazoline is used to prevent nose bleeds if the nasal route is chosen. This technique requires thorough application of topical anesthesia to the airway. There are numerous ways to accomplish this task. The topical anesthetic of choice is plain lidocaine, as the complication of methemoglobinemia with benzocaine can obscure the clinical picture during airway management and harm the patient [28]. Aerosolization of 4 percent lidocaine to the tongue and oropharynx for an oral intubation, or nasal mucosa and posterior oropharynx for a nasal intubation is sometimes sufficient. Gargling and panting after some lidocaine has accumulated in the posterior oropharynx will facilitate further topicalization of the glottic and subglottic regions. The adequacy of the topical anesthesia can be determined by assessing the patient’s ability to tolerate insertion of an oral airway. If the patient gags, then it is removed, and further lidocaine is applied. Applying lidocaine specifically to the airway below the vocal cords may not be necessary if the patient has managed to aspirate some lidocaine while panting. A transtracheal instillation of lidocaine may be performed, however. This technique is particularly useful for diminishing coughing once the endotracheal tube is inserted and its cuff inflated. With this technique, a skin wheal is made directly over the cricothyroid membrane with 1 percent lidocaine. A 20 G angiocatheter is then attached to a syringe containing lidocaine. The angiocatheter is advanced through the membrane while withdrawing on the plunger of the syringe. When air is aspirated in the syringe, the angiocatheter is advanced, and the needle is removed. The syringe is then attached directly to the catheter, and lidocaine is instilled. This technique may be safer than direct instillation via a needle, as the chance of coughing and movement at the time of lidocaine administration is high. Topicalization of an airway is time-consuming and difficult to accomplish in some patients who are particularly anxious or uncooperative. If such a patient is an appropriate candidate for bag mask ventilation, then fiberoptic intubation may be accomplished after induction of anesthesia. The fiberoptic intubation, whether awake or asleep, can be accomplished either from the head of the bed, or at the side of the patient. It is appropriate to develop proficiency with both techniques, as situations such as chin-on-chest deformity may require fiberoptic intubation from the side. Anesthetic Technique Most surgery for spine trauma carries with it significant risk of blood loss. An arterial catheter is therefore appropriate, as it allows serial measurements of hematocrit, as well as continuous

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blood pressure monitoring (see Chapters 4 and 5). In addition, the respiratory variation of the arterial line, or reversed pulsus paradoxus, [29] is a useful indicator of a volume responsive state [30]. In patients who were otherwise healthy prior to their injury and who do not require ongoing inotropic or vasopressor support at the time of surgery, an arterial line may be the only invasive monitor necessary. In large thoracic or lumbar spine surgeries, particularly in the prone position, central venous access is warranted. In addition to providing more access for volume resuscitation, transducing a central venous pressure (CVP) is helpful for monitoring filling pressures of the right heart. The value of the CVP is controversial, however. It does allow calculation of ocular perfusion pressure (OPP = MAP – CVP). Although there are currently no data to support the notion that an adequate ocular perfusion pressure decreases the incidence of postoperative visual loss, maintaining an ocular perfusion pressure of 60 mmHg is reasonable. In addition, in the absence of traumatic brain injury, an ocular perfusion pressure in this range should also ensure an adequate cerebral perfusion pressure (CPP, which can also be calculated as the difference of mean arterial pressure and CVP unless intracranial pressure is elevated, in which case CPP = MAP – intracranial pressure). The CVP is not a useful measure for determining volume status, however; it is neither a good indicator of preload nor a predictor of cardiac function in response to volume administration [31]. Although some literature suggests a benefit to managing older patients with trauma with a pulmonary artery catheter, [32] its use certainly cannot be routinely recommended (see Chapter 5). A recent large study has demonstrated that the complications associated with pulmonary artery catheter use are similar to those of central line placement [33]. Therefore, although there may be few clear indications for their use, placement of a pulmonary artery catheter can certainly be justified in sick patients with poor cardiac function, especially in those in whom fluid management is difficult and vasopressor therapy is required. The recent development of arterial line-based cardiac output monitoring may diminish the need for pulmonary artery catheter use, however. Neuromonitoring The goal of surgery in the setting of SCI is not only to stabilize the spinal column, but also to prevent further injury to the cord. Unfortunately, the surgery itself, such as achieving fracture reduction or placing hardware, has potential for causing further injury. Intraoperative neuromonitoring is frequently performed in order to minimize further risk to the cord (see Chapter 5). Several modalities are used commonly, and each has specific anesthetic implications. The general term for this type of neuromonitoring is evoked potential monitoring. A small stimulus is applied to the patient, it is transmitted through a specific pathway in the nervous system, and subsequently measured at its termination, where the continued presence of signal indicates an intact pathway. Because the magnitude of the signal in evoked potential monitoring is so small, summation of successive repetitive signals is necessary in order to distinguish the signal from other electrical activity. Patients with complete SCIs will have no transmission of signal through the lesion, and neuromonitoring is therefore not possible. It is, however, reasonable to perform some baseline

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measurements in patients who are thought to have complete injuries. If some signal persists, then it may be worth the effort to preserve it. Somatosensory evoked potentials (SSEP) are the most common type of intraoperative neuromonitoring for spine surgery. An electrical stimulus is applied peripherally, and the signal is measured by using scalp electrodes over sensory cortex. In the context of spine surgery, SSEP monitoring is useful for confirming the integrity of the posterior column where afferent pathways predominate. A 50 percent decrease in the amplitude of the signal associated with a surgical intervention is considered clinically significant and should cause the surgeon to revise the ongoing surgical plan. In addition, a 10 percent increase in signal latency probably shares the same significance. Volatile anesthetics decrease amplitude and increase latency in a dose-dependent manner. In addition, nitrous oxide also impairs signal amplitude. If only SSEP monitoring is performed, then low-dose volatile anesthetic combined with generous opioid supplementation is a reasonable anesthetic technique. SSEP is also well preserved with intravenous anesthetics, even in the setting of EEG burst suppression. A total intravenous anesthetic (TIVA) is therefore an appropriate alternative to volatile anesthetic. Because SSEP only detects injury to the sensory pathways of the spinal cord, isolated injury to descending pathways could potentially be missed. Motor evoked potentials (MEPs) have become an increasingly common technique for detecting injury to efferent motor tracts, and thereby complement SSEP for spinal cord monitoring. This technique involves depolarization of the motor cortex via transcranial electrical or magnetic stimulation. The latter method is not feasible for intraoperative monitoring, however, so electrical stimulation is used exclusively. Electromyographic potentials are then recorded over muscles in the lower extremities. The MEP is much more sensitive to the effects of anesthetics than SSEP. TIVA is essential for adequate signal quality. A continuous infusion of propofol with either remifentanil, sufentanil, or fentanyl is appropriate. In addition, neuromuscular relaxants must be avoided. Visual evoked potential monitoring is accomplished through stimulation of the retina with light from light-emitting diodes in goggles worn by the patient, with subsequent measurement of cortical electrical activity. The use of visual evoked potentials for intraoperative monitoring is uncommon because of the profound effect of anesthetics on signal quality. In fact, it has traditionally been viewed as a useless intraoperative device [34]. Recent concern over postoperative visual loss has prompted exploration of its application to prone spine surgery, however. Although not an evoked potential, spontaneous electromyography (EMG) can be monitored simultaneously with SSEP and MEP. This technique relies on the strong motor activity that occurs when a nerve root is irritated by the surgeon. EMG in an adequately anesthetized patient should be minimal, but surgical contact with a large peripheral nerve should stimulate activity. This monitoring modality is particularly useful in either cervical or lumbar spine surgery, when the surgeon is working around nerve roots that form either the brachial plexus or lumbar sacral plexus. Anesthetic considerations include avoidance of neuromuscular relaxants.

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Patient Positioning Patient positioning for spine surgery requires the same careful attention to pressure-point padding and neutral extremity positioning as with any surgery (see Chapter 16). The prone position is somewhat more difficult to achieve satisfactory padding, however. Whether using the Mayfield device to hold the head in pins or a prone pillow, it is essential to be certain that there is no pressure on the globes or nose. The pillow may move over time, and the eyes should be checked periodically. In addition, slight reverse Trendelenburg may facilitate venous drainage from the head and reduce congestion and intraocular pressure [35]. Padding on the chest must not creep up and compress the neck, as this too may obstruct venous drainage. Other areas of concern in positioning include the breasts, which may suffer from pressure necrosis, and the male genitalia, which should not be compressed. The knees and toes also are at risk for pressure sores. Temperature Regulation Due to loss of cutaneous vasomotor tone below the level of their lesions, patients with SCI have difficulty with thermoregulation and are therefore at risk of developing hypothermia in the acute period. Although there is evidence that mild to moderate hypothermia in the setting of central nervous system injury decreases mediators of secondary injury, [36] there is yet no clear evidence for therapeutic hypothermia in SCI patients (see Chapter 29). Therefore, these patients should be kept normothermic. The problem of poikilothermia in SCI presents no new challenges to the anesthesiologist, however, because all patients become so when maintained on a volatile anesthetic. Glucose Management Tight glycemic control has become the standard of care in critically ill surgical patients following a prospective study in 2001, which demonstrated both a mortality and morbidity benefit from maintenance of serum glucose between 80 and 110 mg/dL [37]. In addition, hyperglycemia is deleterious in the setting of traumatic brain injury [38]. Apart from animal model data, [39] there is little information regarding the effect of hyperglycemia on SCI. Without compelling evidence to the contrary, it is reasonable to assume that hyperglycemia is as harmful in SCI as brain injury. Many patients with SCI become hyperglycemic either from the stress of the injury or from the subsequent effects of methylprednisolone. As such, insulin should be used in these patients for aggressive glucose management while these patients are in the ICU, and probably also while they are in the operating room. Goals for glucose management in the operating room are difficult to define, however. The prospective studies on glucose management have been in the ICU setting. There is a paucity of outcome data on intraoperative glucose control in patients undergoing noncardiac surgery. Any intervention in this setting must weigh the risks of insulin therapy against the potential benefits of euglycemia. Again, there is little published literature on either side of this issue. Given the clear association between hyperglycemia and harm in central nervous system injury, which is likely true of the spinal cord as well, admin-

istering insulin via a continuous infusion is probably indicated if serum glucose levels are checked sufficiently often to avoid hypoglycemia. In major spine surgeries, where frequent blood gas analyses are performed, achieving glucose levels below 140 mg/dL, and even as low as 110 mg/dL, is reasonable.

C O M P L I C AT I O N S O F A N E S T H E S I A F O R S P I N E S U R G E RY Postoperative Visual Loss Although there are many potential complications of spine surgery, including massive hemorrhage, venous air embolism, myocardial infarction, pulmonary edema, and pressure necrosis, the complication of postoperative visual loss is of particular concern in prone spine surgery, although it can occur in other settings [40] (see Chapter 23) The visual loss is commonly bilateral and due to ischemic optic neuropathy, although retinal artery occlusion and cortical blindness may also occur [41]. These incidents of visual loss occur despite the absence of pressure on the eyes from positioning errors. Ischemic optic neuropathy is associated with blood loss and hypotension, but most certainly has a multifactorial etiology, including anatomic variation in the vasculature of individual patients [42]. Given the increasing recognition of this problem, determining whether a patient has experienced any visual changes is an integral part of the postoperative evaluation. Visual complaints warrant an immediate ophthalmology consult. Late Issues of Spinal Cord Injury Muscle denervation via SCI results in rapid up-regulation of acetylcholine receptor isoforms across the muscle belly, not just localized to the neuromuscular junction, which are stimulated by acetylcholine, succinylcholine, and choline [43]. The profound hyperkalemia that can result from the use of succinylcholine, described by Gronert and Theye [44] in 1975, is potentially lethal. Although it is unclear at what point succinylcholine use becomes unsafe, it is probably appropriate to avoid it after 48 hours postinjury (see Chapter 9). Although the return of spinal cord reflexes following SCI mitigates the problems of hypotension and orthostasis, a new problem, that of autonomic hyperreflexia, also arises several months after injury. Autonomic hyperreflexia is more commonly a problem in persons with SCI above T6. It is characterized by episodes of profound hypertension, which likely results from unmodulated sympathetic discharge originating below the lesion in the cord as a result of sensory stimulation. It may also be accompanied by baroreflex-mediated bradycardia. Although it can arise intraoperatively, as a result of surgical stimulation, deepening the anesthetic is therapeutic.


1. Concerning spinal cord injuries: a. In patients sustaining a spinal column fracture, the incidence is ≤6% in a Canadian study. b. They are more common in women than men.

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c. Motor vehicle collisions are an unlikely mechanism of injury. d. The presence or absence of osteoporosis is unlikely to affect the incidence. 2. Identify the correct statement regarding anatomy of the spinal cord a. It is made up of 8 cervical, 11 thoracic, 5 lumbar and sacral segments. b. The anterior two-thirds of the spinal cord is supplied via the anterior spinal artery, which arises from the intercostal arteries. c. The artery of Adamkiewicz is an important radicular artery providing blood to the thoracolumbar cord. d. The cord terminates at approximately L4 in adults. For questions 3–6, match the statement with the correct answer.

S TAT E M E N T S

3. Associated with worsening of original injury (secondary injury) 4. Spinal cord injury without radiographic abnormality 5. Central cord syndrome 6. Brown–Séquard syndrome a. Occurs more commonly in children than adults b. Hypotension due to hemorrhage or loss of systemic vasomotor tone c. Increased upper- versus lower-extremity weakness, associated with bladder dysfunction, and variable loss of sensory function below the lesion. d. Loss of motor and touch sensation ipsilateral to the lesion, with pain and temperature sensation lost contralateral to the lesion.

ANSWERS

1. a 2. c

3. b 4. a

5. c 6. d

REFERENCES

1. Hu R, Mustard CA, Burns C. Epidemiology of incident spinal fracture in a complete population. Spine 1996;21(4):492–9. 2. Dryden DM, Saunders LD, Rowe BH, May LA, Yiannakoulias N, Svenson LW, Schopflocher DP, Voaklander DC. The epidemiology of traumatic spinal cord injury in Alberta, Canada. Can J Neurol Sci 2003;30(2):113–21. 3. Pickett GE, Campos-Benitez M, Keller JL, Duggal N. Epidemiology of traumatic spinal cord injury in Canada. Spine 2006;31(7):799–805.

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20. Bracken MB, Shepard MJ, Collins WF, Holford TR, Young W, Baskin DS, Eisenberg HM, Flamm E, Leo-Summers L, Maroon J, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 1990;322(20):1405–11. 21. Sayer FT, Kronvall E, Nilsson OG. Methylprednisolone treatment in acute spinal cord injury: The myth challenged through a structured analysis of published literature. Spine J 2006;6(3):335–43. 22. Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, Cottingham R, Svoboda P, Brayley N, Mazairac G, Laloe V, Munoz-Sanchez A, Arango M, Hartzenberg B, Khamis H, Yutthakasemsunt S, Komolafe E, Olldashi F, Yadav Y, MurilloCabezas F, Shakur H, Edwards P; CRASH trial collaborators. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): Randomised placebo-controlled trial. Lancet 2004;364(9442):1321–8. 23. Edwards P, Arango M, Balica L, Cottingham R, El-Sayed H, Farrell B, Fernandes J, Gogichaisvili T, Golden N, Hartzenberg B, Husain M, Ulloa MI, Jerbi Z, Khamis H, Komolafe E, Laloe V, Lomas G, Ludwig S, Mazairac G, Munoz Sanchez Mde L, Nasi L, Olldashi F, Plunkett P, Roberts I, Sandercock P, Shakur H, Soler C, Stocker R, Svoboda P, Trenkler S, Venkataramana NK, Wasserberg J, Yates D, Yutthakasemsunt S; CRASH trial collaborators. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injuryoutcomes at 6 months. Lancet 2005;365(9475):1957–9. 24. Guest J, Eleraky MA, Apostolides PJ, Dickman CA, Sonntag VK. Traumatic central cord syndrome: Results of surgical management. J Neurosurg 2002;97(1 Suppl):25–32. 25. McKinley W, Meade MA, Kirshblum S, Barnard B. Outcomes of early surgical management versus late or no surgical intervention after acute spinal cord injury. Arch Phys Med Rehabil 2004;85(11):1818–25. 26. Harris MB, Sethi RK. The initial assessment and management of the multiple-trauma patient with an associated spine injury. Spine 2006;31(11 Suppl):S915. 27. Fehlings MG, Perrin RG. The timing of surgical intervention in the treatment of spinal cord injury: A systematic review of recent clinical evidence. Spine 2006;31(11 Suppl):S28–35. 28. Ash-Bernal R, Wise R, Wright SM. Acquired methemoglobinemia: A retrospective series of 138 cases at 2 teaching hospitals. Medicine (Baltimore) 2004;83(5):265–73. 29. Massumi RA, Mason DT, Vera Z, Zelis R, Otero J, Amsterdam EA. Reversed pulsus paradoxus. N Engl J Med 1973;289(24): 1272–5. 30. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005;103(2):419–28.

31. Kumar A, Anel R, Bunnell E, Habet K, Zanotti S, Marshall S, Neumann A, Ali A, Cheang M, Kavinsky C, Parrillo JE. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004;32(3):691–9. 32. Friese RS, Shafi S, Gentilello LM. Pulmonary artery catheter use is associated with reduced mortality in severely injured patients: A National Trauma Data Bank analysis of 53,312 patients. Crit Care Med 2006;34(6):1597–601. 33. Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D, Brampton W, Williams D, Young D, Rowan K; PAC-Man study collaboration. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): A randomised controlled trial. Lancet 2005;366(9484):472–7. 34. Cedzich C, Schramm J, Mengedoht CF, Fahlbusch R. Factors that limit the use of flash visual evoked potentials for surgical monitoring. Electroencephalogr Clin Neurophysiol 1988;71(2):142–5. 35. Ozcan MS, Praetel C, Bhatti MT, Gravenstein N, Mahla ME, Seubert CN. The effect of body inclination during prone positioning on intraocular pressure in awake volunteers: A comparison of two operating tables. Anesth Analg 2004;99(4):1152–8. 36. Fritz HG, Bauer R. Secondary injuries in brain trauma: Effects of hypothermia. J Neurosurg Anesthesiol 2004;16(1):43–52. 37. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001;345(19):1359–67. 38. Jeremitsky E, Omert LA, Dunham CM, Wilberger J, Rodriguez A. The impact of hyperglycemia on patients with severe brain injury. J Trauma 2005;58(1):47–50. 39. Sala F, Menna G, Bricolo A, Young W. Role of glycemia in acute spinal cord injury. Data from a rat experimental model and clinical experience. Ann N Y Acad Sci 1999;890:133–54. 40. Roth S, Gillesberg I. Injuries to the visual system and other sense organs. In Benumof JL, Saidman LJ, ed. Anesthesia and Perioperative Complications, 2nd edition. St. Louis: Mosby, 1999, pp 377–408. 41. Myers MA, Hamilton SR, Bogosian AJ, Smith CH, Wagner TA. Visual loss as a complication of spine surgery. A review of 37 cases. Spine 1997;22(12):1325–9. 42. Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995;80(5):1018–29. 43. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: Etiologic factors and molecular mechanisms. Anesthesiology 2006;104(1):158–69. 44. Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology 1975;43(1):89–99.

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15 M U S C U L O S K E L E TA L T R AU M A Heather A. Vallier and Mark D. Jenkins Objectives 1. Define goals in the management of musculoskeletal trauma. 2. Discuss the potential advantages and disadvantages of early fracture fixation. 3. Describe patient and injury characteristics necessary to formulate a treatment plan. 4. Develop treatment strategies for urgent and emergent musculoskeletal problems.

G E N E R A L A P P R OAC H T O M U S C U L O S K E L E TA L T R AU M A C A R E Introduction Trauma is the leading cause of death and disability in the United States in people under the age of 45 years, accounting for more than 100,000 deaths each year, and annual medical expenses of more than $200 billion [1–3]. Most trauma-related deaths are associated with closed-head injuries or exsanguination shortly after the injury. Patients who survive the initial traumatic event are at risk for various life-threatening complications, many of which are directly related to their musculoskeletal injuries. Trauma care is evolving to address the initial musculoskeletal insult and treat or avoid secondary complications. Essential goals of treatment include resuscitation, pain relief, improved stability and alignment, enhanced mobility, and ultimately restoration of function. Goals of Treatment Resuscitation The American College of Surgeons Committee on Trauma has developed Advanced Trauma Life Support (ATLS) protocols to aid in the initial evaluation and resuscitation of the trauma patient [4]. These validated protocols are practiced at trauma centers throughout the United States and involve primary, secondary, and tertiary surveys of the patient. The primary survey is a stepwise evaluation of airway, breathing, circulation, disability, and exposure. This primary survey is followed by a secondary survey in which a detailed history and physical examination is completed. The tertiary survey involves serial evaluations of the patient’s status during their hospital course. Initial evaluation will identify the location and severity of injuries and determine the patient’s physiologic status,

including the presence of shock. There are four types of shock: hypovolemic, cardiogenic, obstructive, and distributive. Musculoskeletal injuries are associated with hemorrhage. Hypovolemic shock is most frequently encountered in trauma patients, especially those with pelvis and long-bone fractures. Shock results in tissue hypoperfusion, hypoxemia, activation of the inflammatory cascade, and immune dysfunction [86]. Reduction and fixation of fractures will generally promote control of hemorrhage and the pathophysiology of shock, aiding in the resuscitation of the patient. Pain Relief Pain is a patient’s essential early-warning system that an injury has occurred. It is an invaluable tool that can be used to identify injuries in the multiple-trauma patient, especially during the secondary and tertiary surveys. Painful stimuli from an injury aid in diagnosis of the problem and initiation of treatment, so that further damage of the surrounding structures can be avoided. Despite these beneficial aspects of pain, pain induces sympathetic discharge that can contribute to a hyperinflammatory response, increasing the risk of morbidity and mortality in severely injured patients [5]. Pain also leads to splinting and impaired ventilation, which causes atelectasis. Atelectasis may result in hypoxemia or pneumonia. Additionally, pain can adversely affect the outcome of an injury by becoming the primary focus of the patient and their family. Uncontrolled and constant pain contributes to continued immobility leading to thromboembolic events, decreased motion, pulmonary complications, and even death. Therefore, prompt yet judicious pain control is critical in the care of the multiply injured patient (see Chapter 34). Pain control can be achieved by several different methods. Fracture stabilization, whether provisional or definitive, will provide some pain relief. Reduction of dislocated joints significantly 225

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decreases pain. These and other interventions combined with various medications including nonsteroidal anti-inflammatory drugs, opiates, analgesics, antidepressants, and anticonvulsants can be used effectively to maximize patient comfort and recovery. Stability and Alignment Early stabilization and restoration of alignment of fractures is an essential step in the resuscitation and pain relief of trauma patients. Unstable pelvis, acetabulum, and femur fractures are often definitively managed within the first 24 hours [6–10]. The urgency and type of stabilization varies among different types of injuries and will depend on the overall status of the patient. It ranges from a simple splint placed in the field providing axial stability to early appropriate operative care restoring fracture alignment and placing complex implants. General principles of management for long-bone fractures, like the tibia and femur, include correction of longitudinal, angular, and rotational malalignment. Definitive treatment is frequently with intramedullary nails, but plates and external fixators can also be used to accomplish these goals. Articular fractures, involving joint surfaces, demand strict attention to anatomic reduction and rigid internal fixation, commonly with plates and screws. These procedures are often undertaken on a delayed basis, several days or even weeks after injury, to allow for swelling around the fracture to decrease, reducing the risk of wound-healing problems and infections [11, 12]. Provisional external fixation spanning the injured joint is frequently done to control fracture alignment and to provide pain relief for these complex intraarticular lower-extremity fractures. Enhanced Mobility By stabilizing musculoskeletal injuries, a patient’s mobility can be maximized throughout the entire trauma-related event. Improved mobility of the multiply injured patient has positive effects and can start in the field when traction and splints are applied. Even crude initial splints facilitate nursing care and decrease secondary insult due to injury during transport. Definitive stabilization of individual fractures permits a patient to initiate early range of motion of the associated joints and to optimize their flexibility. The benefits of enhanced mobility go beyond the pain relief and obvious functional and psychologic gains. A patient with restored mobility is at decreased risk of venous stasis, deep venous thrombosis, and pulmonary emboli, which can be fatal. Improved mobility decreases the need for continued nursing care, allows for earlier hospital discharge, and ultimately facilitates the return to preinjury level of function. Restoration of Function The ultimate goal of trauma care and intervention is to return the patient to his or her preinjury status. This can involve a simple nonoperative treatment plan or multiple different procedures and possibly a multistaged reconstruction that can take many months. Many patients with multiple injuries do not reach a level of maximal function for up to 24 months. Treatment of musculoskeletal injury thus has a dramatic impact on the patient and society due to the demographics of trauma patients. The typical trauma patient is a young male laborer, contributing significantly to the workforce. In addition to the

direct costs of medical treatment and rehabilitation, indirect costs of lost productivity due to premature morbidity and mortality are substantial. Optimization of all aspects of trauma care will restore function and minimize costs to society. Timing of Musculoskeletal Care Acute versus Subacute Injuries The timing and type of treatment in a patient with multiplesystem trauma and fractures are controversial and should be undertaken in a collaborative fashion with members of the team providing care. Life-threatening and limb-threatening musculoskeletal injuries are addressed emergently. These include patients with massive hemorrhage from pelvic fracture or multiple long-bone fractures, arterial injury in an extremity, and compartmental syndrome. In these situations, orthopedic management contributes to resuscitation and promotes viability of life and limb. Other musculoskeletal injuries should be treated on an urgent basis. These include open fractures, unstable pelvis, acetabulum, or femur fractures, hip fractures, and dislocated joints. Definitive management for most other articular fractures, and isolated extremity injuries can be on a subacute basis. This ensures that the systemic resuscitation for the trauma has been completed, nutrition has been addressed, and underlying medical conditions have been evaluated and optimized. Furthermore, many articular injuries have severe soft tissue swelling that precludes open reduction and internal fixation in the first few days. Extensile surgical approaches for some of these fractures, like the tibial plateau or plafond or the calcaneus, can result in disastrous soft tissue complications and infections [11, 12]. Provisional versus Definitive Fixation The majority of multiply injured patients have musculoskeletal injuries. These and other injuries place the patient at risk for various complications such as fat embolism, adult respiratory distress syndrome (ARDS), and sepsis. Since the introduction and standard practice of early fracture fixation, the benefits have proved to be multifactorial. Many studies have documented the positive effects of early fracture management in reducing morbidity and mortality [6–10, 13–17]. Reduction and stabilization of fractures stops bleeding and provides pain relief. Early fixation allows early and enhanced mobilization, better pulmonary function, improved wound care, diminished wound complications, and ultimately better function. These effects are even more profound in patients with multiple-system injury versus those with an isolated fracture (Table 15.1). In terms of timing, the concept of early fixation has evolved from weeks to hours. In 1982, Goris et al. published a report that supported fixation within the first 24 hours to reduce the morbidity, ARDS, and sepsis rates [13]. Johnson et al. completed a retrospective review of 132 multiple-trauma patients with two major fractures and an Injury Severity Score (ISS) of 18 or greater [9]. They noted an increased incidence of ARDS when fixation was delayed beyond 24 hours. The overall ARDS incidence was 7 percent in the early fixation group versus 39 percent in the group with fixation beyond 24 hours. Early definitive long-bone fixation and external fixation methods have

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Table 15.1: Summary of Some of The Literature Regarding the Timing of Fixation for Unstable Orthopedics Injuries Author

Study Type

Comparison

No. of Patients

Bone et al. [6]

Randomized prospective

Femur fixation ≤24 hours vs. >24 hours

Lozman et al. [41]

Randomized prospective

Femur and tibia treatment immediate, vs. nonop

Seibel et al. [69]

Retrospective cohort

Group 1 = immediate fixation femur or acetabulum and mobilization Group 2 = 10 days of traction postop Group 3 = 30 days of traction postop

56

More pulmonary failure, sepsis, fracture complications, and narcotics usage when mobilization delayed. Supports early fixation.

Pape et al. [52]



106

Patients without concurrent thoracic trauma had shorter intubation time and shorter ICU stay when treated early. Patients with severe chest trauma had more ARDS and mortality with early fixation.

Poole et al. [57]


Femur fixation ≤24 hours vs. >24 hours vs. nonop in patients with head injury

114

Risk of pulmonary complications not related to timing of fixation. No difference in CNS outcomes among the three groups.

Rixen et al. [63]

Review of retrospective studies


1465

The use of provisional or definitive external fixation in these patients increased over this time period and was associated with an increased Injury Severity Score (ISS), a lower Glasgow Coma Scale, thoracic trauma, a base deficit >6.0, or an elevated prothrombin time. However, no advantage to external fixation vs. primary femoral stabilization with a nail or plate was seen.

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Results Fixation after 24 hours associated with more pulmonary complications, greater length of stay, more ICU days, greater costs of care. Supports early fixation. Mean cardiac index higher and mean shunt was lower with immediate fixation. Supports early fixation.

The level of evidence in most studies is poor. The majority of published information to date supports early fixation, although in recent years some authors have questioned this as a routine strategy.

continued to evolve and are now considered to be an integral part of the initial resuscitative care. Although the practice of early fixation continues to be supported by multiple studies, not all traumatologists are in agreement that it is the primary determinant of improved outcomes. With the widespread use of ATLS protocols and the evolution of trauma care, it is clear that improvements in prehospital, resuscitative, and critical care have contributed to decreased morbidity and mortality. Reynolds et al. in a retrospective review of 424 consecutive multiple-trauma patients found that the severity of the injuries and not the timing of fracture fixation

determined the pulmonary outcome [18]. They concluded that clinical judgment was the most important factor regarding the timing of fracture fixation. Decision-Making Process Early fracture stabilization and fixation represents an important shift in the care of multiply injured patients. The majority of current data supports early stabilization when combined with sound clinical judgment (Table 15.1). Many patients are too sick not to operate on. The exact timing of surgical intervention will depend on multiple factors starting with the

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Table 15.2: Estimated Fluid and Blood Loss∗ Class I

Class II

Class III

Class IV

Blood loss (mL)

Up to 750

750–1,500

1,500–2,000

>2,000

Blood loss (% of volume)

Up to 15%

15–30%

30–40%

>40%

Heart rate

≤100

>100

>120

>140

Blood pressure

Normal

Normal

Decreased

Decreased

Pulse pressure (mmHg)

Normal

Decreased

Decreased

Decreased

Respiratory rate

14–20

20–30

30–40

>35

Urine output (mL/hr)

>30

20–30

5–15

Negligible

Mental status

Slightly anxious

Mildly anxious

Confused

Lethargic

Fluid replacement (3:1 rule)

Crystalloid

Crystalloid

Crystalloid and blood

Crystalloid and blood

∗ Reprinted

with permission from Shock, in Advanced Trauma Life Support Student Course Manual, 6th edition. Chicago, IL:, American College of Surgeons, 1997, p 108.

initial injury and management at the scene. The orthopedic surgeon, the trauma critical care team, and the anesthesiologist must work together to decide the appropriate timing of surgical intervention and fracture fixation. Primary Parameters of Trauma Management SCORING SYSTEMS

During the development of our current trauma practices several scoring systems were created and continue to be used today. Some of these scoring systems are first employed in the field and help in injury identification and stratification of polytrauma patients. A commonly utilized example is the Glasgow Coma Scale. It was developed to quantify the severity of head injuries and relies on three examinations, including motor response, verbal response, and eye opening. Other scoring systems incorporating different anatomic and physiologic parameters have been developed. Frequently used systems include the Abbreviated Injury Score (AIS), the ISS, and the Revised Trauma Score (RTS). Depending on the characteristics of each system, they have been used in multiple ways, including patient evaluation, outcome predictions, quality assurance, research, and more recently, hospital reimbursement. Usage of these systems will undoubtedly continue to evolve as our knowledge increases. PHYSIOLOGIC

Many different physiologic parameters are used in the evaluation of the multiply-injured patient. Early and accurate assessment of the cardiovascular system is critical in the care of the trauma patient. Identification and characterization of shock promotes immediate, appropriate intervention. Basic physiologic parameters assessed include the heart rate, blood pressure, temperature, respiratory rate, urine output, and mental status (Table 15.2). Integration of these values can be used to estimate fluid and blood loss. Other more advanced parameters can be obtained, including cardiac output, systemic vascular resistance, pulmonary wedge pressure, central venous pressure, and systolic pressure variability (see Chapter 5). Echocardiography can be used to further define the hemodynamic state (see Chap-

ter 33). These values can be used to differentiate types of shock and to make fine adjustments during volume replacement. L A B O R AT O RY

Several laboratory parameters routinely obtained during care of the multiply injured patient are crucial for appropriate management. In combination with physiologic parameters and physical exam, these are usually sufficient for resuscitation. Severe musculoskeletal trauma and associated hemorrhage result in tissue hypoperfusion, which leads to acidosis. The extent of acidosis can be assessed by determining the pH, lactate, or base deficit. Normalization of these values within 24 hours of injury is predictive of survival. Because pH is less specific and more easily regulated by the body’s compensatory mechanisms, and lactate is subject to confounders such as alcohol ingestion or renal disease, the base deficit is the most reliable indicator of resuscitation. This value can be used as a guide in the volume repletion of the trauma patient [19–22]. Improvement in the base deficit over time is one of the most accurate and specific indicators of a patient’s volume repletion and tissue oxygenation. Secondary Parameters of Trauma Management S O F T T I S S U E : S W E L L I N G , WO U N D S

Many high-energy musculoskeletal injuries are associated with severe soft tissue damage or destruction. Although open fractures and unstable femoral and pelvic fractures are managed urgently, many fractures of the extremities are managed provisionally with splinting or external fixation until the soft tissues have healed sufficiently to tolerate additional surgical incisions [11, 12]. Articular fractures, involving joint surfaces, demand strict attention to anatomic reduction and rigid internal fixation, commonly with plates and screws. Many of these fractures are definitively treated on a delayed basis, several days or even weeks after injury, to allow for swelling around the fracture to decrease. This reduces risks of wound-healing problems and infections. In some cases definitive management is with external fixation, depending on the injury and characteristics of the patient.

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NUTRITION

Adequate nutrition is essential for healing of wounds and fractures. Trauma increases caloric needs, making it difficult to maintain body weight and protein stores during the healing period. The burden of multiple trauma, and the inability to take food by mouth, possibly due to associated injuries, which may necessitate ventilatory support, lead to a catabolic state after injury. Inadequate nutrition is associated with increased risks of infection, wound- and fracture-healing problems, and skin breakdown (decubitus ulcers). Trauma also produces stress, which leads to more gastric acid production and increased intestinal translocation of bacteria. Early enteral nutrition will minimize these issues in trauma patients. Sometimes it is prudent to delay reconstructive procedures associated with fractures until nutrition has been optimized. Two-Hit Model of Organ Dysfunction Trauma management has evolved over time to incorporate models that explain the associated pathophysiology. The two-hit model of organ dysfunction is based on a dysfunctional inflammatory response. In this model, severely injured patients with massive hemorrhage enter a systemic hyperinflammatory state called systemic inflammatory response syndrome (SIRS). The intensity depends on the initial injury, which is described as the first hit. A secondary inflammatory event can result in a secondary insult leading to multiple-organ failure [5, 21– 24]. Orthopedic fracture fixation may contribute to this secondary response in underresuscitated patients, depending on the amount of blood loss generated by surgery. An adequate level of resuscitation is crucial in avoiding this second hit and its adverse consequences. Damage-Control Orthopedics An emerging term related to the two-hit model is damagecontrol orthopedics [25]. This is a concept to provide early fracture stabilization, while minimizing the second hit caused by prolonged surgical procedures [24, 26]. This tactic generally involves avoiding longer definitive procedures with large blood loss, in favor of shorter surgical procedures. An example would be stabilization of a femur fracture with provisional external fixation instead of definitive fixation with an intramedullary nail. Although some studies have suggested decreased initial operative times and less bleeding with a damage-control strategy [24–27], many unstable pelvis and acetabulum fractures can not be provisionally stabilized with external fixation. Furthermore, the need for additional (definitive) surgery on a delayed basis, for example, conversion of a femoral external fixator to an intramedullary nail, and the potential for more complications and costs make this practice controversial. Currently, it is unclear exactly which patients benefit from a damage-control strategy [27].

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and extremities. It will describe mechanisms of injury and resultant pathology and outline initial treatment measures. Lifethreatening and limb-threatening injuries will be reviewed and guidelines for injuries of lesser significance will be explained. Life-Threatening Injuries Musculoskeletal injuries can be life-threatening when they are associated with massive hemorrhage. Bleeding can be due to an isolated fracture or the combination of multiple fractures and blood loss from other body systems. Pelvic fractures or bilateral femur fractures are the two most frequent injuries that can cause bleeding of this magnitude. Usually this bleeding will be into a closed space – not immediately obvious to the examiner. Open fractures with extensive soft tissue destruction and/or arterial injury are another problem that can be not only limbthreatening, but also life-threatening because of the amount of associated hemorrhage. Pelvic Ring Injuries Certain pelvic fractures can be associated with blood loss of several liters. High-energy forces are required to disrupt the stability of the pelvis. Unstable pelvic fractures have mortality rates of 10–21 percent [30–33]. Urgent resuscitation and early stabilization can minimize morbidity and mortality in these patients. A basic understanding of the fracture pattern and the anatomy and mechanics behind it is essential to treating these patients. The pelvis is a bony ring comprising two innominate bones and the sacrum (Figure 15.1). Pelvic stability comes primarily from the posterior sacroiliac complex, providing about 60 percent of the ring stiffness [31, 32, 34]. The pelvic floor and the symphysis pubis also contribute to pelvic stability. Because of its ring structure, if the pelvis is broken in one location, another fracture or dislocation is very likely to be present. Injuries to the pelvic ring may be classified based on the direction of initial impact. Progressive force in a given direction will generate instability of pelvic structures in a predictable fashion. Associated injuries and blood loss correlate with the pattern of pelvic fractures [28, 30, 31, 33, 35].

M U S C U L O S K E L E TA L E M E R G E N C I E S Major orthopedic trauma occurs in almost 80 percent of multiply injured patients. The incidence of orthopedic trauma in these patients is approximately equal to the incidence of head injury, twice that of thoracic injury, and four times that of abdominal injury [8, 29]. The following discussion will provide a basic approach to musculoskeletal trauma including the pelvis

Figure 15.1. The pelvis is a bony ring when viewed from above. Sacroiliac ligaments, sacrospinous ligaments, sacrotuberous ligaments, and the symphysis pubis are important stabilizing elements.

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Lateral Compression

AP Compression (open book) Figure 15.2. Progression of injury to the pelvic ring seen with an anteriorly directed force. Diastasis of the pubis symphysis occurs. Further force causes external rotation of each hemipelvis, disrupting the posterior pelvic ring. With increased displacement of the posterior pelvic ring, more bleeding will occur.

Anteroposterior injuries are due to direct force to the anterior pelvis or external rotation force to the hemipelvis through the femur. These commonly occur in head-on motor vehicle accidents or in crush injuries. Forces “open” the anterior pelvic ring by externally rotating the innominate bones. The pubic symphysis may fracture and widen – a so-called open-book pelvis fracture – and/or the pubic rami may fracture (Figures 15.2 and 15.3). Continued forces produce fractures and dislocations to the posterior pelvic ring, ultimately resulting in displacement of one or both hemipelves. The amount of bleeding associated with a pelvic fracture is frequently related to the amount of displacement of the posterior pelvic ring [28, 30, 33]. Because a single pelvis radiograph depicts only one point in time, it does not necessarily demonstrate the degree of displacement that occurred at the time of the accident. A high index of suspicion for significant bleeding is essential when the diagnosis of an open-book pelvic fracture is made. Prompt

Figure 15.4. Progression of injury to the pelvic ring seen with a laterally directed force. Progressive force causes disruption of the ipsilateral posterior pelvic ring in the form of a dislocation and/or fracture. With continued force, the contralateral hemipelvis will experience an external rotation deformity.

physiologic assessment for hemodynamic instability and physical examination to evaluate pelvic stability are imperative. Lateral compression injuries are due to lateral impact to the pelvis. Frequently this happens in a motor vehicle accident or a fall onto the side. Impaction of the sacrum on the side of the forces is usually seen, along with pubic ramus fractures, as the affected hemipelvis internally rotates (Figure 15.4). This is the most common pelvic fracture pattern. Progressive force can completely destabilize the affected hemipelvis, producing a sacroiliac dislocation or fracture-dislocation. The contralateral hemipelvis can become unstable, rotating externally. Blood loss and neurologic injuries are generally related to the magnitude of displacement of the posterior pelvic ring, although massive hemorrhage is much less likely with this injury pattern compared with an open-book fracture [28, 30, 32, 36, 37]. Lastly, so-called vertical shear injuries are caused by axial force to the pelvis. This is often the result of a fall from a height or a motorcycle accident. The affected hemipelvis will be displaced superiorly, creating instability of the posterior pelvic ring (Figure 15.5). Concomitant stretching of the lumbosacral plexus and vascular structures are not infrequent with this fracture pattern (Figure 15.6).

Vertical Shear Figure 15.3. Anteroposterior pelvis radiograph demonstrates an openbook pelvis fracture, with widening of the symphysis pubis and complete dislocation of the right sacroiliac joint.

Figure 15.5. An axial force to the pelvis causes significant instability of the pelvic ring due to injuries of the pubic symphysis or rami as well as the entire posterior ligamentous complex. The magnitude of posterior pelvic ring injury correlates with the amount of bleeding.

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Aorta Common iliac aa. Middle sacral a. Iliolumbar a. Lumbosacral trunk Ext. iliac a. Umbilical & sup. vesical a.

S1

Obturator a.

S3

Visceral aa.

S2

Sup. gluteal a. Lat. sacral a.

S1 Inf. gluteal a.

Int. pudendal a.

Figure 15.6. Contents of the pelvis in midline sagittal section. Note the proximity of the lumbosacral plexus and major vascular structures to the posterior aspect of the pelvic ring.

Other musculoskeletal injuries occur with 60–80 percent of pelvic ring fractures [28–30]. Severe open-book pelvic fractures and vertical shear fracture patterns are often associated with other injuries. With each of these types of pelvic fracture, the pelvic fracture has a high propensity to cause massive hemorrhage. In contrast, lateral-compression pelvic ring fractures are not associated with as much bleeding, thus associated head injuries and abdominal injuries are potentially more problematic than the pelvic fracture. Whitbeck et al. [33] described forty-three patients with complete disruption of the sacroiliac joint and a mortality rate of 21 percent. Half of these patients died of massive hemorrhage, while 25 percent of the fatalities were secondary to traumatic brain injury, and the other 25 percent were due to multiple-organ failure over the first several days. To minimize mortality, acute management of unstable pelvic fractures must first address bleeding. Open fractures, urogenital trauma, and gastrointestinal injury in conjunction with pelvic fractures are very infrequent and are also considered surgical emergencies. Bleeding is the most frequent initial problem associated with pelvic fractures. Three sources of bleeding may be seen: bony, venous, and arterial. Blood loss secondary to the fractured bone surfaces is usually insignificant. However, the proximity of major branches of the iliac vessels to the sacroiliac joints results in bleeding when the posterior pelvic ring is displaced. (Figure 15.6) Bleeding from the sacral venous plexus can be extensive, with blood loss of up to 3–10 L. The retroperitoneum of the intact pelvis can hold 4 L of blood before tamponade occurs. As the pelvis is shaped like a cone, the volume available for blood to accumulate is proportionate to the radius cubed. Initial management should consist of provisional reduction of open-book patterns (reducing the size of the pelvis radius) by manually closing the pelvic ring with a sheet or binder [38]. This decreases pelvic volume and can help to tamponade bleeding from the sacral plexus. Very rarely there is major arterial injury associated with fracture of the pelvic ring. This occurs in about 6–8 percent of unstable pelvic fractures [35, 39]. Angiography and embolization or pelvic packing are life-saving measures in these patients. If the patient is unresponsive and severely

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hypotensive, despite aggressive fluid replacement and pelvic reduction, emergent angiography should be performed (Figure 15.7). Urgent surgical interventions in patients with unstable pelvic fractures are aimed at provisional or definitive reduction and stabilization of the pelvic ring. This promotes tamponade by reducing the bleeding bone surfaces and decreasing the pelvic volume to a normal level. Fortunately, modern techniques of surgical stabilization for sacroiliac dislocations and fracture-dislocations often may be performed percutaneously with fluoroscopic assistance in the supine position [40]. This minimizes surgical time and blood loss. Reduction and stabilization of the anterior pelvic ring are usually performed during the same surgical procedure (Figure 15.8). Whenever possible, expeditious definitive management is undertaken [10, 28, 35]. This may consist of open reduction and internal fixation of a symphyseal disruption or anterior pelvic external fixation [86]. Special mention should be made of open pelvic fractures. In addition to the pelvic ring injury and associated hemorrhage and neurologic insult, visceral injuries are more common, and a high rate of infection is seen. Historically, mortality of open pelvic fractures approached 50 percent [41–45]. Control of bleeding is the most important initial measure, followed by debridement and packing of open wounds. Patients with posterior or perineal wounds or rectal trauma are treated with a diverting colostomy [46, 47]. Extraperitoneal bladder tears are repaired. A team approach, including anesthesia, general surgery, orthopedics, urology, and gynecology, is essential in the management of these complex, often critically ill patients [35]. Long-Bone Fractures Life-threatening hemorrhage can occur with bilateral femoral shaft fractures or multiple long-bone fractures. Mortality rates of up to 25 percent have been reported in this population [48, 49]. Although this group of patients is likely to have major injuries to other systems, which would increase their mortality risk, the hemorrhage associated with multiple long-bone fractures is impressive. Immediate treatment measures should be undertaken when these patients are identified. Central intravenous access or a minimum of two large-bore intravenous lines are recommended. The average blood loss associated with a femoral shaft fracture is 1,500 cc, and with a humeral shaft fracture or a tibial shaft fracture it is 750 cc. This does not include additional bleeding associated with surgery. Frequently the fracture hematoma is within a closed space, not immediately obvious to the examiner, which can result in a dangerous delay in resuscitation. Most femoral and tibial shaft fractures in adults are definitively treated with reamed intramedullary nailing. Unstable femoral fractures are usually fixed in the first 24 hours to reduce the risk of associated pulmonary complications [6]. Stabilization eliminates the need for skeletal traction and recumbency. It also provides control of bleeding from the fracture and thus is considered part of a multiply injured patient’s resuscitation. During surgery, careful monitoring by the anesthesia team is crucial. Adjunctive volume replacement will depend on the pattern and number of fractures, as well as other injuries contributing to bleeding. Isolated femoral shaft fractures may be treated on a fracture table in a lateral or supine position, depending on sur-

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Unstable pelvic ring fracture

ATLS protocol, 2L iv fluid bolus, Closed reduction of pelvis with sheet ± traction SBP≥100mmHg

SBP Provide extra runners > Provide extra nursing for blood drawing or screening

4 pRBC 4 FFP 1 6pk platelets 90 MINUTES 4 pRBC 4 FFP

4 FWB

120 MINUTES

PROTOCOL TERMINATED WHEN NO LONGER NEEDED

Figure 22.2. Example of massive transfusion protocol. A whole-blood drive could be called if the attending surgeon or anesthesiologist decided this was appropriate. Injury patterns of two limbs plus a body cavity were an indicator that whole blood would probably be needed as was ongoing transfusion of greater than 20 units of packed cells, 20 units of plasma, and other components. pRBC, packed red blood cells; FWB, fresh whole blood; FFP, fresh-frozen plasma; cryoppt, cryoprecipitate; RTD, return to duty; DCCS, damage control casualty station; CSH, Combat Surgical Hospital.

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Figure 22.5. An soldier who suffered bilateral traumatic amputations of the upper extremities above the elbow during Operation Iraqi Freedom has his pain managed with bilateral infraclavicular brachial plexus catheters. Photo courtesy of Army Regional Anesthesia & Pain Management Initiative.

Figure 22.3. An Iraqi patient undergoes surgery on a traumatically amputated thigh while spontaneously ventilating. He did not have any regional anesthetic and is receiving a titrated mixture of propofol, ketamine, and fentanyl mixed in one bag. Photo courtesy of C. McFarland.

Figure 22.6. Equipment needed for single injection or continuous regional techniques. The StimuQuik™ insulated peripheral nerve block needle by Arrow®, the Contiplex® Tuohy Continuous Nerve Block Set by B-Braun, and the PainPump2® by Stryker® are among the equipment shown. Photo courtesy of C. McFarland.

Figure 22.4. Equipment required for the Field TIVA technique described in the box. The medications are propofol, fentanyl, and ketamine. The drip set is 20 drops per milliliter. No anesthesia machine, infusion pumps, batteries, or electricity are required to deliver an anesthetic in this manner, resulting in minimal logistical impact. Photo courtesy of C. McFarland.

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Figure 23.3. An open-eye injury resulting from trauma from a racquet.

Figure 22.7. Dr. Malchow uses a portable ultrasound to facilitate femoral nerve block in a patient with external fixation of his femur. Photo courtesy of R Malchow.

Figure 27.1. Full thickness facial laceration through parotid duct. Note the difficulty in identification of the duct within the laceration.

Figure 23.2. Conjunctival laceration with subconjunctival hemorrhage. This is an example of a closed-eye injury.

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Figure 27.2. Propofol used to identify the duct after cannulation through the mouth. Figure 27.4. After tracheostomy and flap reflection, extensive soft tissue, hard tissue, and dentoalveolar trauma is seen.

Figure 27.5. Complex scalp degloving injury in a unhelmeted motorcyclist. Figure 27.3. Complex lower facial soft tissue trauma after GSW.

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Figure 27.13. Intraoral view of patient in trauma bay.

Figure 27.6. Tissue realigned, and rotational flaps utilized.

Figure 27.14. Clinical view of patient with maxillomandibular fixation in place. Figure 27.7. Primary repair of scalp laceration.

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Figure 27.15. A, View of GSW patient in trauma bay. Patient intubated by Life Flight prior to arrival. B, Significant hard and soft tissue damage to lower jaw, extraoral view. C, Intraoral view of maxillary injuries.

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Figure 27.20. Clinical view of patient in trauma bay with extensive midface trauma. Figure 27.17. Six weeks postoperative view of patient with external pinfixation/distractor in place.

Figure 27.18. Clinical view of patient with right orbital floor fracture, with restricted superior gaze.

Figure 27.23. Surgical exposure of a patient with a commented frontal sinus fracture.

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COLD INJURY

CELLULAR EFFECTS OF COLD

+–– – ++

THAW

LATE Extracellular +/– intracellular H2O crystallization

EARLY

Cellular dysfunction

Membrane damage Water leaves cells

Inceased extracellular fluid

Cell death

SYSTEMIC EFFECTS OF COLD

Electrolyte imbalance

Cognitive dysfunction, delirium, aphasia amnesia, coma

Modified protein structures

J waves, decreased contractility, bradycardia, arrhythmia

THERMOREGULATORY RESPONSE

V/Q mismatch

Hypertension, tachycardia

Shock

Ileus

Rewarming shock

Cold diuresis, renal failure

Bladder atony Shivering Peripheral vasoconstriction

Rhabdomyolysis

Bullae

TISSUE EFFECTS OF COLD Neuropathy

Stasis

Gangrene Endothelial injury

Interstitial edema Lactic acidosis

Hemoconcentration Thrombosis

Vascular insufficiency Figure 29.13. Cold-induced injuries such as hypothermia and frostbite lead to thermoregulatory response (e.g., shivering and increased sympathic activity), cellular and tissue effects (e.g., membrane damage, electrolyte imbalance, endothelial injury, and thrombosis) and systemic effects (e.g., shock, arrhythmia, and neuromuscular dysfunction). Reproduced with permission from reference 30.

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Figure 31.3. Ultrasound-guided supraclavicular block.

A

Figure 31.4. Ultrasound guided infraclavicular block. B

Figure 31.12. Surgeon-proof dressing.

Figure 31.8. Tunneling of catheter.

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Figure 32.2. Supraclavicular sonogram of neural elements (n) adjacent to subclavian artery (SCA).

Figure 32.8. Sonographic anatomy of the brachial plexus in the interscalene region: Scalenus medius (SM), scalenus anterior (SA), and sternomastoid muscle (SM). Superior (s), middle (m), and inferior (i) trunks.

Figure 32.10. Sonographic anatomy of the brachial plexus in the infraclavicular region, medial to the coracoid.

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Axillary Vessels Nerve Axillary artery Axillary vein

Median Nerve

Coracobrachialis Musculocutaneous nerve Ulnar nerve

Radial nerve

Musculocutaneous nerve

Vein

Nerves

Figure 32.11. Sonographic anatomy of the brachial plexus in the axillary region.

Figure 32.12. Diagram of cross-section at the cubital fossa showing relations of radial, median, and ulnar nerves.

Figure 32.14. Sonographic anatomy of the femoral nerve below the inguinal ligament.

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A

B Figure 35.7. Thermography of the hand. (A) Computerized telethermography. (Left) Dorsal hands, (Right) palmer hands. (B) Liquid crystal thermography. (Left) Dorsal hands, (Right) palmar hands. From Edwards BE, Hobbins WB. Pain management and thermography. In Gay SM, ed. Practical Management of Pain, 2nd edition. St Louis: Mosby-Year Book, 1992, pp 168–84, with permission.

C

D

Figure 35.8. Example of lumbar plexus block. (C) Representation of the innervation of the lumbar plexus that originates between L1-L2 and L5-S1 and ultimately forms the major branches of the plexus, which include the genitofemoral nerve through the obturator nerve. (D) Demonstration of the lumbar plexus block technique that involves advancing the needle 4 cm lateral to the spine at the level of the iliac crest. From Hadzic AJ, Vloka JD. Peripheral Nerve Blocks. New York: McGraw–Hill, 2004, pp 219–23, figures 18.2 and 18.7, with permission.

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Intraspinal Catheter Pump

B

A

C

D

Figure 35.10. Implantable devices are often effective in treating severe and refractory pain conditions, including complex regional pain syndrome (CRPS) and other neuropathic pain syndromes. Due to their invasive nature, associated complications and expense, these devices are typically third-line treatments. (A) Implanted spinal cord stimulator and the course of the lead in the epidural space. (B) The course of an implanted intrathecal pump. (C) The actual implantation of an intrathecal pump. (D) Radiograph of a patient with an implanted intrathecal pump. Figure 10A and B from Medtronic, with permission.

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B

C

D

E

F

Figure 35.15. Kyphoplasty. (A) The blunt dissector and the working cannula are introduced using a pedicular approach. (B) The deflated balloon tamp is passed down the working cannula under fluoroscopic control. (C) Inflation of the balloon tamp and reduction of the fracture. (D) Deflation of the balloon tamp. (E) Application of the cement. (F) Removal of the working cannula. From Daniel S, Daisuke T, Isador HL. Kyphoplasty: Vertebral augmentation for compression fractures. Clin Geriatr Med 2006;22:535–44, with permission.

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Figure 18.11. Anatomy of the intercostal space. Intercostal nerve block is done at the site of thoracic pain and one to two segments above and below by using local anesthetics such as bupivacaine or ropivacaine. Note the location of the intercostal nerve (N) in relation to the artery (A) and vein (V). With continuous infusions, local anesthetic can spread to adjacent spaces. Extent of spread is volume dependent. Sinatra RS, Ennevor SJ. Trauma patient with thoracic and abdominal injuries. In Rosenberg AD, Grande CM, Bernstein RL, ed. Pain Management and Regional Anesthesia in Trauma. London: WB Saunders, 2000, p 314.

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Postoperative Considerations Following Cardiothoracic Trauma After cardiothoracic trauma, patients often require support of the respiratory and cardiovascular systems and optimization of oxygen delivery in the ICU. Care is directed toward management of general problems such as fluids, pain control, nausea and vomiting, head injuries, agitation, and complications of unsuspected drug abuse. Serial CXRs, assessment of chest tube drainage, and monitoring for complications related to the initial trauma such as pulmonary contusion, blunt cardiac injuries, retained hemothorax, empyema, pulmonary cavitary lesions, and noncardiothoracic injuries (e.g., head, spinal cord, abdominal, retroperitoneal, orthopedic, and vascular injuries) may be necessary. Specific postcardiothoracic trauma complications include ARDS, multiple organ system failure, and sepsis, the last two being the major late causes of death in trauma. In patients with traumatic lung injury, the incidence of ARDS, empyema, recurrent pneumothorax, pneumonia, bleeding/hemothorax requiring reoperation, and mortality have been found to be higher with blunt injuries (versus penetrating), low blood pressure at thoracotomy, and increasing amount of the lung resection [64]. Postoperative complications after cardiac trauma include intracardiac shunts, valvular lesions, ventricular aneurysms, wall-motion abnormalities, arrhythmias, and conduction blocks. Retained foreign body and aortocaval and aortopulmonary fistula may also occur in survivors of penetrating cardiac trauma. S U M M A RY ■

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Figure 18.12. Transverse section at the level of the intervertebral foramen showing the relation of the intrapleural space to the rib and intercostal nerve. Local anesthetic diffuses from the pleural space through the parietal pleura and the intercostal muscle to block the intercostal nerve. Orliaguet G, Carli P. Thoracic blocks. In Rosenberg AD, Grande CM, Bernstein RL, ed. Pain Management and Regional Anesthesia in Trauma. London: WB Saunders, 2000, p 242.

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With severe blunt trauma, the heart and great vessels are most often disrupted at one of four “anchor points”: the aortic root, the posterior left atrium, the cavoatrial junction in the right atrium, and the proximal descending thoracic aorta. Blunt trauma can cause myocardial contusion, most often to the right ventricle, which can present as hypotension and/or arrhythmia. Diagnostic findings that tend to confirm this diagnosis include cardiac isoenzyme elevations, ECG changes, and TEE changes, but there is no “gold standard” for diagnosis of this entity. Penetrating wounds to the heart most often injure the right ventricle and carry a high mortality, especially with gunshots. The cause of death is either exsanguination or cardiac tamponade. Aortic disruptions typically occur at the attachment site of the ligamentum arteriosum in the proximal descending aorta. These often cause immediate exsanguination, but life can be spared if the aortic adventitia or parietal pleura contains the rupture, in which case downstream ischemia to abdominal organs and to the spinal cord can result from decreased aortic blood flow before or during surgical repair. Surgical and anesthetic management of descending thoracic aortic traumatic disruptions is complex and typically involves partial left heart bypass and the use of lung isolation. Avoidance of hypertension and tachycardia through the use of several possible pharmacologic interventions probably reduces the chance of free

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rupture into the hemithorax before the surgeon can gain control of the injured aorta. Blast injury can cause several different types of trauma, but the most common thoracic injury is barotrauma leading to pneumothorax, so early chest tube insertion is often critical for those who acutely survive the blast. Air embolus is the most frequent cause of death.


1. Which of the following cardiothoracic anatomic locations is NOT an anchor point subject to avulsion from deceleration forces during an automobile accident? a. b. c. d. e.

Junction between vena cavae and right atrium Posterior left atrium Proximal descending aorta Aorta at diaphragmatic hiatus Mitral valve annulus

2. A 21-year-old unrestrained driver experiences a deceleration injury with his chest against a steering wheel in an automobile that lacks an air bag. ST segments are abnormal in leads V1 and V2 and plasma troponin I levels are increased. A chest x-ray shows a fluffy “butterfly” central infiltrate pattern, sternal fracture, and prominent pulmonary vascular markings. The mediastinum and cardiac silhouette appear normal. Which of the following pathologic combinations is most likely? a. Pulmonary contusion and right ventricular dysfunction b. Thoracic aortic dissection and pulmonary edema. c. Left anterior descending coronary rupture and left ventricular failure d. Aortic root (proximal ascending aorta) rupture and pericardial effusion e. Pulmonary arterial injury and left ventricular contusion 3. A 42-year-old man who was in a domestic dispute has a butcher knife sticking out of his chest. The knife is going straight into the parasternal portion of the left fifth intercostal space. Which of the following cardiac structures is most likely to be injured? a. b. c. d. e.

Interventricular septum Lateral wall of right atrium Anterior wall of right ventricle Left anterior descending coronary artery Apex of left ventricle

4. An unidentified and unconscious young man presents to the emergency room with a bullet entry wound in the right anterior fourth intercostal space and an exit wound in the left posterior paraspinous muscles at approximately T8. Blood pressure, 70/50; heart rate, 110; respiratory rate, 28 per minute; SPO2 , 92 on face mask O2 . After placing bilateral chest tubes and intubation, the next action should be a. Obtaining a chest x-ray b. Performing a transthoracic echocardiogram

c. Obtaining a thoracic CT scan d. Placing a radial arterial catheter e. Change to a double-lumen endobronchial tube 5. In a blunt deceleration-type injury, the most common site for aortic disruption is a. Aortic valve b. Junction of ascending aorta and innominate artery c. Junction of subclavian artery and descending thoracic aorta d. Diaphragmatic hiatus e. Bifurcation of abdominal aorta 6. The most common outcome of a traumatic aortic rupture is a. b. c. d. e.

Long-term survival with medical management Long-term survival with immediate surgical repair Long-term survival with elective surgical repair Delayed death from pseudoaneurysm rupture Immediate death

7. Which of the following diagnostic modalities is LEAST specific for diagnosing a suspected acute traumatic rupture of the descending thoracic aorta? a. b. c. d. e.

Magnetic resonance imaging Spiral CT scan Transesophageal echocardiography Chest x-ray Aortography

8. A 32-year-old man will soon undergo anesthesia for repair of a traumatic dissection of the proximal descending aorta. He has received morphine sulfate 14 mg intravenously, which has reduced his back pain from a score of 10 of 10 to 4 of 10, and he is now sleepy unless stimulated. His blood pressure is 174/102, heart rate is 105, and respiratory rate is 12 per minute. Which of the following interventions is most appropriate at this time? a. Initiate a nitroglycerin infusion IV b. Place a thoracic aortic catheter and administer epidural ropivacaine c. Administer additional morphine IV d. Administer a dexmedetomidine loading dose IV e. Initiate esmolol and nitroprusside IV infusions 9. A 22-year-old woman was near an outdoor explosion and was thrown against a wall. She never lost consciousness. Physical examination reveals impaired hearing, bruises on her back, and no other obvious injuries. She is conscious, dyspneic, and apprehensive. Blood pressure, 90/60; heart rate, 110; respiratory rate, 32 per minute; room air SPO2 , 86 percent without splinting or an obvious flail chest. Breath sounds are present but somewhat diminished bilaterally. After administering oxygen by face mask, your next action should be a. Intubate and initiate positive pressure ventilation b. Perform a transthoracic echocardiogram

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c. Insert bilateral chest tubes d. Perform a tracheostomy e. Order a chest x-ray 10. A 25-year-old man experienced blunt trauma from a blast injury 1 hour ago. A transthoracic echocardiogram reveals a large pericardial effusion with diastolic invagination of the right ventricle. Other diagnostic studies have ruled out pleural effusion and intraabdominal blood. A subxiphoid pericardial window is planned. Blood pressure, 80/50; pulse, 120; respiratory rate, 28 per minute. Which of the following anesthetic options is most appropriate? a. Rapid sequence induction and intubation followed by positive pressure ventilation b. Administration of nitrous oxide analgesia (60% N2 O, 40% O2 ) by face mask c. Local anesthesia for the surgical field accompanied by intravenous sedation using midazolam d. Placement of a laryngeal mask airway under propofol anesthesia with attempts to preserve spontaneous ventilation e. Thoracic epidural anesthesia

ANSWERS

1. 2. 3. 4.

e a c b

5. c 6. e 7. d

8. e 9. c 10. c

REFERENCES

1. Lockey D, Crewdson K, and Davies G. Traumatic cardiac arrest: Who are the survivors? Ann Emerg Med 2006;48(3):240–4. 2. Orliaguet G, Ferjani M, Riou B. The heart in blunt trauma. Anesthesiology 2001;95(2):544–8. 3. Bertinchant JP, Robert E, Polge A, et al. Release kinetics of cardiac troponin I and cardiac troponin T in effluents from isolated perfused rabbit hearts after graded experimental myocardial contusion. J Trauma 1999;47(3):474–80. 4. Pretre R, Chilcott M. Blunt trauma to the heart and great vessels. N Engl J Med 1997;336(9):626–32. 5. Sutherland GR, Calvin JE, Driedger AA, et al. Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury. J Trauma 1981;21(1):1–12. 6. Robert E, de La Coussaye JE, Aya AG, et al. Mechanisms of ventricular arrhythmias induced by myocardial contusion: A highresolution mapping study in left ventricular rabbit heart. Anesthesiology 2000;92(4):1132–43. 7. Chirillo F, Totis O, De Cavarzerani A, et al. Usefulness of transthoracic and transoesophageal echocardiography in recognition and management of cardiovascular injuries after blunt chest trauma. Heart 1996;75(3):301–6. 8. Wall MJ Jr, Mattox KL, Chen CD, et al. Acute management of complex cardiac injuries. J Trauma 1997;42(5):905–12. 9. Degiannis E, Loogna P, Doll D, Bonnano F, Bowley DM, Smith MD. Penetrating cardiac injuries: Recent experience in South Africa. World J Surg 2006;30(7):1258–64.

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10. Hunt PA, Greaves I, Owens WA. Emergency thoracotomy in thoracic trauma-a review. Injury 2006;37(1):1–19. 11. Lim R, Gill IS, Temes RT, Smith CE. The use of adenosine for repair of penetrating cardiac injuries: A novel method. Ann Thorac Surg 2001;71:1714–5. 12. Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997;336(26):1876–88. 13. Williams JS, Graff JA, Uku JM, Steinig JP. Aortic injury in vehicular trauma. Ann Thorac Surg 1994;57(3):726–30. 14. Fann JI, Miller DC. Aortic dissection. Ann Vasc Surg 1995;9(3): 311–23. 15. Ledbetter S, Stuk JL, Kaufman JA. Helical (spiral) CT in the evaluation of emergent thoracic aortic syndromes. Traumatic aortic rupture, aortic aneurysm, aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. Radiol Clin N Am 1999;37(3):575–89. 16. Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography. Anesth Analg 1999;89(4):870–84. 17. Karski JM. Transesophageal echocardiography in the intensive care unit. Semin Cardiothorac Vasc Anesth 2006;10(2):162–6. 18. Burns JM, Sing RF, Mostafa G, Huynh TT, Jacobs DG, Miles WS, Thomason MH. The role of transesophageal echocardiography in optimizing resuscitation in acutely injured patients. J Trauma 2005;59(1):36–40; discussion 40–2. 19. Ben-Menachem Y. Assessment of blunt aortic-brachiocephalic trauma: Should angiography be supplanted by transesophageal echocardiography? J Trauma 1997;42:969–72. 20. Eggebrecht H, Nienaber CA, Neuhauser M. Endovascular stentgraft placement in aortic dissection: A meta-analysis. Eur Heart J 2006;27(4):489–98. 21. Karmy-Jones R, Hoffer E, Meissner M, Bloch RD. Management of traumatic rupture of the thoracic aorta in pediatric patients. Ann Thorac Surg 2003;75(5):1513–7. 22. Murphy MB, Murray C, Shorten GD. Fenoldopam: A selective peripheral dopamine-receptor agonist for the treatment of severe hypertension. N Engl J Med 2001;345(21):1548–57. 23. Nichols AJ, Ruffolo RR Jr, Brooks DP. The pharmacology of fenoldopam. Am J Hypertens 1990;3(6 Pt 2):116S–9S. 24. Halpenny M, Rushe C, Breen P, et al. The effects of fenoldopam on renal function in patients undergoing elective aortic surgery. Eur J Anaesthesiol 2002;19(1):32–9. 25. Gilbert TB, Hasnain JU, Flinn WR, et al. Fenoldopam infusion associated with preserving renal function after aortic crossclamping for aneurysm repair. J Cardiovasc Pharmacol Ther 2001;6(1):31–6. 26. Papia G. Klein D, Lindsay TF. Intensive care of the patient following open abdominal aortic surgery. Curr Opin Crit Care 2006;12(4):340–5. 27. Sheinbaum R, Ignacio C, Safi HJ, Estrera A. Contemporary strategies to preserve renal function during cardiac and vascular surgery. Rev Cardiovasc Med 2003;4(Suppl 1):S21–8. 28. Oliver WC Jr, Nuttall GA, Cherry KJ, Decker PA, Bower T, Ereth MH. A comparison of fenoldopam with dopamine and sodium nitroprusside in patients undergoing cross-clamping of the abdominal aorta. Anesth Analg 2006;103(4):833–40.

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50. Besson A, Saegesser F. Color Atlas of Chest Trauma and Associated Injuries. Oradell, NJ: Medical Economics Books, 1983, pp 12–14. 51. Hanowell LH. Perioperative anesthetic management of thoracoabdominal trauma. In Grande CM, ed. Textbook of Trauma Anesthesia and Critical Care. St Louis: Mosby-Year Book Inc., 1993, pp 559–82. 52. Ho AM-H, Ling E. Systemic air embolism after lung trauma. Anesthesiology 1999;90:564–75. 53. Ho AM, Lee S, Tay BA, Chung DC. Lung isolation for the prevention of air embolism in penetrating lung trauma. A case report. Can J Anaesth 2000;47:1256–8. 54. Schaefer SD. The treatment of acute external laryngeal injuries. Arch Otolaryngol Head Neck Surg 1991;117:35–9. 55. Meredith JW, Riley RD. Injury to the esophagus, trachea, and bronchus. In Mattox KL, Feliciano DV, Moore EE, ed. Trauma, 4th edition. New York: McGraw-Hill, 2000, pp 473–82. 56. Jewett BS, Shockley WW, Rutledge R. External laryngeal trauma analysis of 392 patients. Arch Otolaryngol Head Neck Surg 1999;125:877–80. 57. Raoof S. Role of bronchoscopy in modern medical intensive care unit. Clin Chest Med 2001;22:241–61. 58. Devitt JH, Boulanger BR. Lower airway injuries and anaesthesia. Can J Anaesth 1996;43:148–59. 59. Brasel K, Stafford RE, Weigelt JA, et al. Treatment of occult pneumothoraces from blunt trauma. J Trauma 1999;46:987–99. 60. Cohn SM. Pulmonary contusion: A review of the clinical entity. J Trauma 1997;42:973–9. 61. Schweiger JHW. The pathophysiology, diagnosis and management strategies for flail chest injury and pulmonary contusion: A review. Anesth Analg 2001 Review Course Lectures: 86–93. 62. Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the respiratory distress syndrome. N Engl J Med 1998;338:347–54. 63. Eberhard LW, Morabito DJ, Matthay MA, et al. Initial severity of metabolic acidosis predicts the development of acute lung injury in severely traumatized patients. Crit Care Med 2000;28:37–47. 64. Karmy-Jones R, Jurkovich J, Shatz DV, et al. Management of traumatic lung injury: A western trauma association multicenter review. J Trauma 2001;51:1049–53. 65. Cogbill TH, Landercasper J. Injury to the chest wall. In Mattox KL, Feliciano DV, Moore EE, ed. Trauma, 4th edition. New York: McGraw-Hill, 2000, pp 483–505. 66. Jougon J, Gallon P, Dubrez J, Velley JF. Perforation oesophagienne au decours de l’echocardiographie transesophagienne. Arch Mal Coeur Vaiss 2000;93:1235–7. 67. Vezina D, Lessard MR, Bussieres J, Topping C, Trepanier CA. Complications associated with the use of the esophageal-tracheal Combitube. Can J Anaesth 1998;45:76–80. 68. Branthwaite MA. An unexpected complication of the intubating laryngeal mask. Anaesthesia 1999;54:166–7. 69. Bulger EM, Arneson MA, Mock CN, Jurkovich GJ. Rib fractures in the elderly. J Trauma 2000;48(6):1040–7. 70. Karmakar MK, Ho AM-H. Acute pain management of patients with multiple fractured ribs. J Trauma 2003;54(3):615–25. 71. Alexander JQ, Gutierrez CJ, Mariano MC, et al. Blunt chest trauma in the elderly patient: How cardiopulmonary disease affects outcome. Am Surg 2000;66:855–7. 72. Mackersie RC, Shackford SR, Hoyt DB, et al. Continuous epidural fentanyl analgesia: Ventilatory function improvement with

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CM, Bernstein RL, ed. Pain Management and Regional Anesthesia in Trauma. London: WB Saunders, 2000, pp 239–51. 75. Sinatra RS, Ennevor SJ. Trauma patient with thoracic and abdominal injuries. In Rosenberg AD, Grande CM, Bernstein RL, ed. Pain Management and Regional Anesthesia in Trauma. London: WB Saunders, 2000, pp 310–38.

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19 I N T R A O P E R AT I V E O N E - L U N G V E N T I L AT I O N F O R T R AU M A A N E S T H E S I A George W. Kanellakos and Peter Slinger Objectives 1. Review the indications for one-lung ventilation in trauma. 2. Describe the physiologic effects of one-lung ventilation in trauma. 3. Review the modern management of one-lung ventilation, including treatment for intraoperative hypoxemia. 4. Discuss lung isolation techniques and relevant bronchial anatomy. 5. Discuss the advantages and disadvantages of equipment options for achieving lung isolation.

INTRODUCTION Trauma patients that have thoracic injuries are extremely difficult to manage and require great expertise with careful clinical management [1]. Other major injuries may be present and management is made much more difficult by the urgency of the situation. The traditional classification of blunt versus penetrating thoracic trauma is important and both mechanisms can lead to significant respiratory injury, at any level within the tracheobronchial tree [2]. Nevertheless, all trauma algorithms place the utmost emphasis on establishing a safe airway. In thoracic trauma, this airway often means having the ability to establish one-lung ventilation (OLV). LU N G I S O L AT I O N I N T R AU M A PAT I E N T S Traditionally, the approach to lung isolation has been divided into absolute and relative indications (Table 19.1) [3]. Within this table, there are two guiding principles that encompass all the indications for OLV. These two categories are: 1. Lung Protection: To prevent contralateral lung soiling against blood or secretions (pus), or to prevent further lung injury secondary to positive pressure ventilation, as in the case of a bronchopleural fistula or severe pulmonary contusion. 2. Surgical Procedures: To facilitate surgical resection. In the case of video-assisted thoracoscopic surgery, it is essential. 300

Both approaches can help guide the clinician, but the decision to establish OLV should be made on a case-by-case basis. If time permits, a discussion with members of the health care team, particularly surgical colleagues, can be very helpful in establishing an agreed upon treatment plan. This is because OLV can be established by a number of techniques that can vary significantly from patient to patient depending on the type of injury, clinical stability, planned surgical procedure, and surgeon preference. One technique is not always the best. In addition, anesthesiologists themselves differ in their approaches, often being influenced by personal experience and comfort levels in various techniques [4]. It is in the best interest of the patient that all members of the health care team agree on the indication for OLV, as it can be associated with multiple complications. There are multiple signs and symptoms that may be present to help guide airway management as well as the urgency for intervention [2]. First, the patient’s normal anatomy must be observed to determine whether intubation would be difficult without the presenting injuries. Difficult intubations can be unexpected in nontrauma patients and, as is often the case, normal airways become significantly more difficult in trauma situations. The clinician must have secondary and tertiary plans at all times and a thorough working knowledge of the difficult airway algorithm is essential. Second, the presence of hoarseness, stridor, hemoptysis, subcutaneous emphysema, mediastinal emphysema on chest x-ray, or a persistent air leak through a chest tube are all important signs to be recognized as they have a great impact on airway management. These signs can indicate the presence of airway

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I N T R A O P E R AT I V E O N E - L U N G V E N T I L AT I O N

Table 19.1: Indications for Lung Isolation Absolute

Relative

Infection

Surgical exposure

Hemorrhage

High: thoracic aneurysm, dissection, or rupture

Bronchial disruption or fistula

High: pneumonectomy

Unilateral bullous disease

High: upper lobectomy

Lung lavage

Low: esophagectomy

Video-assisted thoracoscopic surgery (VATS)

Low: middle, lower lobectomy

Differential ventilation

Low: thoracoscopy

Adapted from Brodsky JB, Lemmens HJM [3].

disruption and are usually caused when high intrathoracic pressure is exerted against a closed glottis. Management is complicated because the location of the injury is often unknown. This not only makes intubation more difficult, but also emphasizes that visualization of the airway is necessary to avoid further injury [1, 5]. Studies indicate that up to 80 percent of injuries occur within 2.5 cm of the carina, which helps provide an area of focus for the clinician [6, 7]. Even with this knowledge, however, bronchoscopy is necessary for confirmation, and to safely secure the airway in these patients, it is recommended that spontaneous respiration be maintained at least until the airway is definitively secured. However the airway is secured, treatment with a chest tube should be expected as positive pressure ventilation might reveal an undetected injury leading to tension pneumothorax [8–10]. In fact, when there is a high probability of lung injury, for example, when rib fractures are evident, it is prudent that chest drainage tubes be placed prophylactically prior to the initiation of positive pressure ventilation. When the injury is high enough above the carina, establishing OLV is usually not necessary to stabilize the patient, but it may be necessary for the surgical repair. Adequate treatment usually involves passing an endotracheal tube (ETT) past the lesion under direct vision and then ventilating normally. When a bronchial or carinal injury is present, the management becomes far more complicated. As mentioned previously, blind insertion of any tube should be avoided, making the availability of fiberoptic bronchoscopy essential. Even though the presence of blood or secretions can make this very difficult, bronchoscopy should always be attempted, as instituting OLV in these patients can be critical for stabilizing the patient and beginning the healing process. In addition to tracheal or bronchial injuries, OLV is also necessary for other thoracic injuries. Vascular injuries vary significantly in their management and surgical repair is often necessary, especially if arterial in nature. When bleeding occurs within the airway, lung isolation for contralateral lung protection is indicated. Stabilization of the patient often occurs only when OLV is established, but occasionally it is not tolerated and oxygenation is compromised. When OLV cannot be tolerated, many techniques can be instituted to manage hypoxemia and these are described later in this chapter. Occasionally, hypoxemia can only be corrected with intermittent two-lung

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ventilation. Care must be taken to minimize airway pressures because initiating ventilation to the injured lung can produce further injury, including more bleeding, pneumothorax, and air embolism [11–15]. Another approach includes differential lung ventilation, with the injured lung exposed to much lower airway pressures. Aside from lung parenchymal vascular injuries, surgical repair of aortic injuries is occasionally required, although most patients do not survive long enough to tolerate surgical intervention. When they do, they are usually limited to sternotomies for the ascending aorta and thoracotomies for descending injuries. Sternotomies rarely require OLV, but the same is not true for thoracotomies. Surgical repair for descending aortic surgery can greatly benefit from OLV. Esophageal injuries account for the last main category of thoracic trauma that requires lung isolation. Injury here is very uncommon because of the protected location of the esophagus, but it can still occur with penetrating trauma or ingestible agents. Surprisingly, the most common cause for esophageal injury is iatrogenic, accounting for 43 percent of all esophageal injuries [16]. Iatrogenic injuries include nasogastric tube placement, traumatic intubations or transesophageal echocardiography. Surgical repair of midesophageal injuries often requires a thoracotomy approach, where once again OLV is advantageous but not critical to the repair [2]. Another select group of trauma patients that can provide great challenges to the anesthesiologist are patients with cervical spine injury that require lung isolation for thoracic surgical procedures. Often the standard approach of using a doublelumen tube (DLT) in these patients is not feasible, secondary to greater difficulty of insertion relative to normal ETTs. Two common approaches include the use of a bronchial blocker placed through a more easily placed ETT or the placement of a DLT via a tube exchanger technique. This is the ideal scenario that highlights the anesthesiologist’s need to be familiar with multiple lung isolation techniques. O N E - LU N G V E N T I L AT I O N Physiologic Effects Ventilation and oxygenation during OLV are complex topics that are very well described elsewhere [17–19]. To quickly summarize, when compared with normal ventilation, two-lung ventilation in the lateral decubitus position with the chest open results in ventilation–perfusion mismatch. This is mostly due to compression of the dependent lung by gravitational, mediastinal, and abdominal forces resulting in relatively greater ventilation to the nondependent lung. Combined with decreased perfusion to the nondependent lung secondary to gravity, the physiologic state leads to a reduction in Pa O2 and an increased PA-a O2 gradient. When OLV is superimposed, oxygenation is further impaired due to the increased shunt that is created. By not ventilating one lung, one would expect a 50 percent cardiac shunt, but this is not what is observed clinically. The measured Pa O2 decreases far less than predicted and the observed shunt measures only 20–30 percent of the cardiac output. The most significant mechanism that accounts for this observation is hypoxic pulmonary vasoconstriction (HPV). Factors affecting HPV are numerous and beyond the scope of this chapter. In general, the lung responds to atelectasis or a reduction

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Table 19.2: Management of One-Lung Ventilation Step 1: Two-lung ventilation until chest opening Step 2: Assess proper tube placement and patency Step 3: FiO2 at 100% [23, 24] Step 4: Tidal volume ■ Conventional: 8–12 mL/kg ■ Current: 6 mL/kg Step 5: Respiratory rate ■ Conventional: maintain pCO2 = 40 mmHg ■ Current: “permissive hypercapnia” when extreme parameters reached [25–28] Step 6: CPAP of 5–10 cm H2 O to nondependent lung [29–31] ■ May interfere significantly in VATS procedures Step 7: PEEP of 5–10 cm H2 O to dependent lung [22, 32] ■ Harmful if preexisting intrinsic PEEP or auto-PEEP is high [33, 34] Step 8: Increase CPAP to nondependent lung to 10–15 cm H2 O Step 9: Equalize PEEP to dependent lung and CPAP to nondependent lung Step 10: Intermittent ventilation of nondependent lung Step 11: HFV to nondependent lung [35] ■ Although superior to CPAP, not practical due to complexity Step 12: Inhaled nitric oxide ■ Benefit limited to patients with pulmonary hypertension [36] Step 13: Pulmonary artery compression CPAP, continuous positive air pressure; HFY, high frequency ventilation; PEEP, peak end-expiratory pressure; VATS, video-assisted thoracoscopic surgery. Adapted from references 17 and 20.

in Pa O2 by increasing pulmonary vascular resistance, leading to a reduction of blood flow through the non-ventilated or “hypoxic” lung. Clinically, this results in most patients easily tolerating the V/Q mismatch introduced by OLV. In addition, there are numerous interventions that can be applied to help reduce the degree of hypoxemia (see next section). It should be noted that most problems regarding OLV revolve around hypoxemia, while the Pa CO2 is significantly less affected as a result of oxygen–hemoglobin dissociation characteristics. Management of One-Lung Ventilation and Hypoxemia Classic management of one-lung ventilation has been described well by Benumof [17, 18, 20]. There have been important updates to this approach and Table 19.2 is a summary of conventional and current management techniques, adapted from modern studies and sources. Of all the interventions listed, the most important maneuver after ensuring an FiO2 of 100 percent is the application of continuous positive airway pressure (CPAP) to the nondependent lung. It is extremely rare for severe hypoxemia (Pa O2 < 50 mmHg) not to be corrected when CPAP is applied [17, 21, 22]. In the operative setting, it is always good practice to discuss starting CPAP with surgical colleagues because it often produces minor expansion of the isolated lung. Many CPAP equipment systems have been described in the literature. Figure 19.1 is an example of the three components that are common to all of these systems. These include an oxygen source, a pressure regulator, and a manometer to measure the resulting pressure.

Figure 19.1. Components of CPAP systems. Three components of continuous positive airway pressure systems: (1) oxygen source, (2) pressure regulator (relief valve), and (3) pressure manometer [20].

Volume Control vs. Pressure Control Although there have been numerous advances in equipment, one of the most important advances in OLV strategies lies in ventilatory management. It has become more and more evident over the past ten years that traditional OLV strategies, particularly ventilatory tidal volumes of 10 mL/kg with respiratory rates of 8–12 breaths per minute, may actually contribute to lung injury [37, 38]. Most patients who are relatively healthy and require OLV are easily managed by using these traditional volume control settings, and this has been the standard of care for thoracic anesthesia. However, the concept of “volutrauma” to a healthy lung can no longer be ignored and many studies have shown that healthy lungs ventilated in this manner do release inflammatory mediators that are commonly seen in patients with acute respiratory distress syndrome (ARDS) [39– 45]. The current debate is whether this is clinically significant [46, 47]. Nevertheless, as a result, many authors advocate that lung-protective strategies currently used to treat ARDS patients should be applied to patients undergoing OLV [48–50]. Practically, this translates to much lower tidal volumes of 6 mL/kg or lower with respiratory rates adjusted to maintain normocapnia. In difficult ventilatory cases, an increase in pCO2 or “permissive hypercapnia” has become an acceptable approach to help limit the degree of lung injury secondary to volutrauma [51]. In addition to the suggested decreased tidal volumes and airway pressures, it should be noted that there are significant differences in the ventilation pattern between volume control ventilation (VCV) and pressure control ventilation (PCV) settings. For any given tidal volume in VCV, the same volume can be achieved in PCV with significantly lower airway pressures [49, 52]. This is due to the mechanical delivery characteristics of each mode of ventilation and the interaction with lung compliance. In healthy patients not undergoing OLV, this is usually not significant because airway pressure seldom becomes elevated. However, in thoracic surgical patients undergoing thoracotomies in the lateral position, airway pressures using VCV can rise significantly. Peak airway pressures of 30 cm H2 O and plateau pressures of 20 cm H2 O are relatively common occurrences. These pressures should trigger the attending anesthesiologist to make adjustments, primarily by converting to PCV.

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Table 19.3: Common Options for Lung Isolation Options

Advantages

Double-lumen tube 1. Direct laryngoscopy 2. Via tube exchanger 3. Fiberoptically

■ ■ ■ ■ ■ ■ ■

Bronchial blockers (BB) 1. Arndt 2. Cohen 3. Fuji 4. Fogarty catheter

■ ■ ■ ■ ■ ■ ■

Univent

■ ■

Disadvantages

Quickest to place successfully Repositioning rarely required Bronchoscopy to isolated lung Suction to isolated lung CPAP easily added Can alternate OLV to either lung easily Placement still possible if bronchoscopy not available

■

Size selection rarely an issue Easily added to regular ETT Allows ventilation during placement Easier placement in patients with difficult airways and in children Postoperative two-lung ventilation easily accomplished by withdrawing blocker Selective lobar lung isolation possible CPAP to isolated lung possible

■

Same as bronchial blockers Less repositioning than BBs

■

■ ■ ■ ■

■ ■ ■ ■ ■ ■

■ ■

Endobronchial tube

■ ■ ■ ■

Endotracheal tube advanced into bronchus

■

Like regular ETTs, easier placement in patients with difficult airways Longer than regular ETT Short cuff designed for lung isolation Tube is reinforced

■

Easier placement in patients with difficult airways

■

■ ■

■ ■

Size selection more difficult Difficult to place in patients with difficult airways or abnormal tracheas Nonoptimal postoperative two-lung ventilation Laryngeal trauma Bronchial trauma

More time needed for positioning Repositioning needed more often Bronchoscope essential for positioning Nonoptimal right lung isolation due to RUL anatomy Bronchoscopy to isolated lung impossible Minimal suction to isolated lung Difficult to alternate OLV to either lung Same as bronchial blockers ETT portion has higher air flow resistance than regular ETT ETT portion has larger diameter than regular ETT Bronchoscopy necessary for placement Does not allow for bronchoscopy, suctioning, or CPAP to isolated lung Difficult right lung OLV Does not allow for bronchoscopy, suctioning, or CPAP to isolated lung Cuff not designed for lung isolation Extremely difficult right lung OLV

CPAP, continuous positive air pressure; ETT, endotrachial tube; OLV, one-lung ventilation.

LU N G I S O L AT I O N T E C H N I Q U E S Innovative and progressive thinkers in lung isolation have benefited the modern day anesthesiologist with a surplus of options for establishing lung isolation. What once was a major undertaking has now become routine and should be part of the skills of all modern day anesthesiology trainees. The options more commonly available are summarized in Table 19.3. It is up to the anesthesiologist to be familiar with these choices, but their availability varies according to institution preference and budget. Although double-lumen tubes might be standard in most institutions, more specialized equipment may not be available or may be used so infrequently that clinicians are uncomfortable with its use. Most clinicians would agree that the gold standard for establishing OLV is with a DLT, as compared with the main alternative, bronchial blockers (BBs). This is based primarily on the assumption that the quality of OLV is best when a DLT is used. In the past this would have been considered true, but both types of technology have undergone major improvement in their design, making the quality of lung isolation between the

two indistinguishable in many cases [53]. In trauma patients, DLTs become less ideal for lung isolation due to their size and difficulty with placement in patients with compromised airways. In these patients, BBs are more easily placed and become more suitable despite their limitations. These limitations must be considered, however, because the placement of a bronchial blocker might be exceptional and provide excellent lung collapse, but it quickly becomes useless if suctioning the isolated lung is essential. The pros and cons of each device must be considered to choose the optimal technique for lung isolation. Provided that institutions are equipped appropriately, it has been suggested that the major barrier to establishing and maintaining lung isolation today is not the choice of equipment, but rather the operator’s limited knowledge of bronchial anatomy [54]. Without proper knowledge of bronchial anatomy, bronchoscopic placement of any endobronchial tube or device is set up for failure from the outset. Despite user preference and bias, and contrary to popular belief, most equipment choices for lung isolation work very well but fail when used inappropriately or used in nonoptimal clinical situations. For example, successful

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DLT placement may be impossible when the anesthesiologist fails to recognize anatomic variations in bronchial segments, such as a carinal right upper lobe take-off. The failure to recognize anatomic features and their interaction with lung isolation equipment is a major barrier to successful lung isolation. Bronchial Anatomy As mentioned, knowledge of bronchial anatomy is critical if lung isolation is to be successfully completed. Unfortunately, it is a subject that is not well emphasized in medical education and is even neglected to some degree in anesthesiology residency training. Although, in theory, the knowledge is easily grasped, applying or correlating that knowledge during handson bronchoscopy is difficult and requires practice. A thorough working knowledge of bronchial anatomy allows troubleshooting of problems with OLV far more efficient and safe. There are a number of anatomic structures that must be familiar to the bronchoscopist. Table 19.4 is a summary of these structures with a few clinical points that can be used to help identify them. Fiberoptic Bronchoscopy Fiberoptic bronchoscopy has become a vital component in providing anesthetic care to thoracic surgery patients. Although proper functioning of endobronchial devices can be verified clinically, their proper placement and/or evaluation during procedures can only be accomplished with bronchoscopy [55]. In addition, the placement of some devices, for example, the Arndt endobronchial blocker, is totally dependent on the use of a fiberoptic bronchoscope. For these reasons, every surgical procedure that requires lung isolation must have a bronchoscope readily available. As with most procedures, to troubleshoot difficult clinical scenarios, the clinician must be totally familiar with normal anatomy and tube placement. This is especially true when anatomic variations arise. It is recommended that all clinicians take every opportunity to practice bronchoscopy and identify the anatomy whenever possible. Bronchoscopy does not only mean becoming familiar with tracheobronchial anatomy, the operator must also anticipate practical problems that arise with everyday use. Other primary reasons for technique failure are inexperience and insufficient planning [1]. For example, during the placement of a bronchial blocker, the operator must anticipate that an adult bronchoscope will not be useful if the patient has a 7.0-mm endotracheal tube in place. Both the blocker and the adult bronchoscope will not fit simultaneously in this tube. Alternatively, an adult bronchoscope provides exceptional suctioning but will not fit within a 35 Fr DLT. It is therefore always prudent to practice the planned procedure to minimize risk to the patient and damage to equipment. Equipment Table 19.3 is a comparison chart that summarizes the advantages and disadvantages of the common technology available for lung isolation. One of the main concerns of past DLTs and present BBs is the pressure they exert against the bronchus, potentially leading to bronchial injury. A recent study comparing the pressures exerted by the cuffs of modern endobronchial

Table 19.4: Bronchial Anatomy (Supine Patient) Anatomical Structure Trachea and carina 1. Membranous trachea posteriorly (dome-shaped lumen) 2. Bifurcation is sharp 3. First generation bronchi are large and have no bifurcations in sight

Left mainstem bronchus (LMB) 1. Long, average length 5 cm 2. Bifurcation of left upper and lower lobes not visible

Left upper lobe (LUL) and left lower lobe (LLL) bronchi 1. Longitudinal bundles usually more prominent into lower lobe (dashed lines) 2. LLL-LUL carina angled horizontally (∼8–2 clock position) Right mainstem bronchus (RMB) 1. Short, average length 2.5 cm (dashed line) 2. Followed by longer right bronchus intermedius (RBI) 3. Right upper lobe (RUL) bifurcation visible Right upper lobe bronchus (RUL) 1. Characteristic bronchial trifurcation

Right bronchus intermedius (RBI) 1. Longitudinal bundles usually more prominent into right lower lobe (dashed lines in proximal view) 2. Linear alignment of bronchi (dashed line in distal view) 3. Right lower lobe (RLL) with segmental bronchi immediately visible 4. Right middle lobe (RML) with segmental bronchi not visible 5. Angle of RML-RLL carina, if followed proximally, would line up with right upper lobe take-off (not visible in figure)

Comments

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Table 19.5: Recommendations for DLT Size

Males

Height 170 cm 41 Fr

Females

Height 160 cm 37 Fr

A

devices shows that in all instances, these cuffs fail to exert a bronchial wall pressure that exceeds 30 mmHg (Figure 19.2) [67]. This, of course, assumes that cuffs are inflated with the appropriate volumes. Double-Lumen Tubes (DLTs) Bjork and Carlens first described DLTs in 1950 [56]. Today there are many manufacturers of DLTS, and since 1950 there have been many changes made in their design [57, 58]. The most notable change has been the introduction of highly visible, low-pressure cuffs [59]. Today, DLTs are used routinely for lung isolation and are considered the gold standard. Proper sizing is important because tubes that are too small have been associated with iatrogenic injury due to being placed too deep in the airway or by causing bronchial injury secondary to hyperinflated cuffs [60]. Tubes that are too large simply do not fit into the bronchus or cause excessive swelling of the airway due to trauma. A guide to selecting the appropriate size DLT is presented in Table 19.5. Placing a DLT can be challenging at times but it can become significantly more difficult in trauma patients. First, laryngoscopy can be more difficult due to cervical spine considerations and because patients often are uncooperative. Second, the airway itself can be compromised and as DLTs are very large they have a greater probability of causing injury than regular ETTs. The recommended depth of insertion is 29 cm for a patient 170 cm tall [61, 62]. When placed with a blind technique, DLT malposition can occur in approximately 30 percent

150 Pressure (mmHg)

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2

3

4

5

6

7

8

9

10

Cuffvolume (ml)

#35 DLT

#37 DLT

#39 DLT

#41 DLT

Arndt EBB

Cohen EBB

Fuji EBB Figure 19.2. The mean pressures exerted by endobronchial devices on the model bronchus, under static conditions. DLT, double-lumen tube; EBB, endobronchial blocker.

B

Figure 19.3. Correct positioning of right and left double-lumen tubes. (A) Right DLT. Within bronchial lumen, center channel should reveal opening of right bronchus intermedius. Side port should show patent right upper lobe bronchus. The bronchial cuff position should then be checked through the tracheal lumen. (B) Left DLT. Within tracheal lumen, the blue bronchial cuff should be slightly visible.

of patients [63]. Whenever ventilation is impaired, the anesthesiologist must check the position of the tube and deflate the bronchial cuff until the problem has been corrected. It has now become widely accepted that DLT placement should always be accompanied by fiberoptic bronchoscopy [63–65]. It is quickly becoming the standard of care [55]. Figure 19.3 shows the correct placement of right and left DLTs. In the situation where the left mainstem bronchus is injured or is the planned location of surgery, it is advantageous to use a right-sided DLT. Placement of right DLTs is never straightforward, as the positioning must be very precise to avoid obstruction of the right upper lobe (RUL). Clinically, a quick method to correctly place a right-sided DLT involves taking note of the RUL location with fiberoptic bronchoscopy, advancing the DLT past the opening, then slowly retracting the tube while rotating in the direction of the RUL orifice. Correct placement is confirmed when the orifice to the RUL is visible through the side opening of the DLT (Figure 19.3) and when the bronchial cuff is successfully inflated so that the left mainstem bronchus is unobstructed. Anomalous right upper lobe anatomy, estimated in 1 in 250 people, is virtually the sole reason why right DLTs fail in providing adequate lung isolation [66]. The other reason is that the tube is easily dislodged secondary to tube, patient position, or surgical movement. It should be noted that a fiberoptic laryngoscope (i.e., GlideScope, WuScope) has quickly made its way into the practice of many anesthesiologists. It has the ability of converting a difficult intubation into one that is easy to manage, a benefit that can also be applied to thoracic anesthesia. Because DLTs are more difficult to insert and trauma patients present with unique airway challenges, it should be remembered that DLT placement can be facilitated with the use of such a scope. The main difficultly encountered clinically is limited space in mouth opening. In these situations, the problem can almost always be overcome by placing the DLT into the oral cavity prior to inserting the fiberoptic laryngoscope. This decreases the potential for cuff rupture, and when the DLT is shaped with the same curvature as the GlideScope blade, the probability of successful intubation is increased. Again, prior to advancing the DLT past the glottic opening, fiberoptic bronchoscopy is always recommended.

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B

Figure 19.4. Double-lumen tube (“tracheopart”) for patients with tracheostomy. (A) Left DLT. (B) Right DLT. Adapted from www.rusch.com.

Another technique that is commonly used to place DLTs in patients with difficult airways involves the use of an airway exchange catheter. These catheters are discussed in more detail below (see Postoperative Ventilation). One patient group in thoracic trauma requires special consideration. This is the patient with a tracheostomy who occasionally requires lung isolation. There are multiple techniques for establishing OLV in these patients. These options include the placement of a regular ETT through the tracheostomy site with advancement into the appropriate bronchus. An alternative to the regular ETT and a better choice is the endobronchial tube (see Equipment). It has a flexible design and a short, distal cuff that is better suited to lung isolation. The use of a DLT or bronchial blocker through the tracheostomy is an acceptable option, but it must be noted that the bulk of the equipment lies outside the patient and may become cumbersome to manage. It should be noted that DLTs were once available in a short design specifically tailored to the tracheostomy patient (Figure 19.4). Unfortunately, contact with the manufacturer revealed these tubes are no longer available. Bronchial Blockers Bronchial blockers consist of a very thin, relatively stiff “catheter” equipped with an inflatable distal cuff. They are designed to be placed within an endotracheal tube and directed into either lung, depending on the clinical situation. Another approach includes placing the blocker external to the ETT, but this results in more difficult placement for successful lung isolation. An addition benefit of bronchial blocker technology is the ability to provide lobar lung isolation, which is impossible to do with other equipment. Figure 19.2 shows how bronchial blockers, when used appropriately with 7 mL of cuff volume

or less, exert a mean pressure less than 30 mmHg against the bronchus wall [67]. Essentially all models available today have this configuration with some form of modification engineered to help direct the distal tip or balloon. Blockers have many advantages over other choices in achieving lung isolation, which have recently only become significant due to their technological advances. There is a belief that bronchial blockers provide less satisfactory surgical conditions than double-lumen tubes. Many believe this to be true and, in fact, there is probably enough evidence in the literature to support such a claim, but only in certain clinical scenarios. The success rate of adequate lung deflation with BB is dependent on the operative side, for reasons related to anatomy. It has been shown that the quality of lung deflation during video-assisted thoracoscopic surgery (VATS), which requires excellent lung deflation conditions, is equal between left DLTs and left BB when left-sided surgery is undertaken. With respect to right-sided surgery, left DLTs provided surgical conditions that were described as “excellent or fair” for all patients. In contrast, 44 percent of patients who had right-sided surgery and received a right BB had “poor” conditions [68]. This suggests that bronchial blockers placed in the left mainstem bronchus and left DLTs are equally effective in left-sided thoracoscopic surgery and presumably other leftsided thoracic surgical procedures. It should be noted, however, that left BB took nearly twice as long to place correctly compared with left DLTs and were associated with a significantly greater number of malpositions [68]. From this study, it was clear that right DLTs were superior compared with BBs for right-sided lung isolation. The increased length of time to position BBs is due to a number of factors, mainly that there are multiple parts to assemble and directing the tip of the blocker is not always straightforward. Placement is difficult unless a trained assistant is present. This, however, is offset by the ability to continue ventilating the patient. When directing the blocker into the desired bronchus is difficult, one way to increase the likelihood of success is to start with the endotracheal tube extremely high in the trachea. Blocker shafts are relatively stiff and directing the tip is difficult. An ETT close to the carina would require a sharp turn with the stiff blocker, something that is extremely difficult to do with the bronchoscope. By placing the tip of the ETT high in the trachea, a small deflection there translates to an improved ability to direct the distal tip left or right. Table 19.6 is a summary of the pros and cons of a few of the bronchial blockers more commonly available. Endobronchial Tubes Endobronchial tubes are long single-lumen tubes that are wire reinforced. They are equipped with a guiding stylet. They differ significantly from regular ETTs, the main differences being in length and cuff design. Figure 19.5 shows an older version of an endobronchial tube with a cuff similar to that found on regular endotracheal tubes. Newer versions of the tube have cuffs very similar to those found on DLTs, making them far more ideal for lung isolation. Similarly to DLTs, when an endobronchial tube is advanced past the glottic opening, the stylet should be removed and replaced with a fiberoptic bronchoscope. The tube is then advanced to its final location under direct visual guidance. In this case the bronchoscope is essential in helping direct the tube to the appropriate bronchus.

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Table 19.6: Comparison of Common Bronchial Blockers Arndt ■ Center channel for CPAP or suctioning ■ Tip is directed with wire loop tightly wrapped around bronchoscope ■ Wire loop removed through center channel ■ Newer models allow wire loop to be reinserted ■ Spherical or elliptical balloon shape

Fuji ■ Center channel for CPAP or suctioning ■ Tip is directed by torquing the blocker, taking advantage of preformed angle proximal to balloon ■ Spherical balloon shape ■ Same blocker technology from Univent tube

Cohen ■ Center channel for CPAP or suctioning ◦ ■ Tip is directed by turning wheel 90 ■ Tip deflects in the direction of the arrow ■ Spherical balloon shape ■ Caution: Turning wheel excessively can stress the mechanism, causing it to malfunction

Univent Tubes The Univent tube, despite having a BB, deserves to be discussed separately because of its unique structure. As described in Table 19.6, the Univent’s blocker has been removed by the manufacturer and is now available as a separate unit (Fuji Bronchial Blocker). Nevertheless, the original unit is still available and used in many institutions. It has a channel along the main endotracheal tube that holds the blocker, and when the tube is placed in the trachea, the blocker is advanced. It is then directed into the appropriate bronchus under fiberoptic guidance. To help facilitate tip direction, the blocker shaft is rotated

or “torqued” while advancing the blocker into the bronchus. Further facilitation can be achieved by turning the endotracheal tube or the patient’s head to one side. Once in position, this blocker may require less repositioning than the other blockers, possibly due to a relatively more “fixed” position at the tip of its endotracheal tube. As with BBs, the main advantage of the Univent tube is that the blocker can be removed, allowing for easy conversion to postoperative ventilation, if necessary. It must be remembered, however, that for any given size of Univent tube, the outer diameter is significantly greater than for normal

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A

B

C

Figure 19.5. Old (A) versus new (B & C) endobronchial tubes.

endotracheal tubes. This requires the selection of a Univent tube to be smaller, thereby reducing the internal diameter even further and increasing airway resistance.

P O S T O P E R AT I V E V E N T I L AT I O N The clinical management of difficult thoracic surgery cases not only requires careful preoperative planning and technical execution, but patient disposition can be equally as challenging. The anesthesiologist can be faced with difficult management decisions regularly, especially with trauma patients, patients with difficult airways, or patients who have had prolonged surgery and now have airways that are compromised. The decision to extubate these patients is not always clear, and it becomes much more difficult in the presence of a DLT. Even if extubation is not planned, postoperative care in an intensive care unit (ICU) can be complicated by the fact that many of the caregivers are not familiar with ventilatory management of a patient with a DLT. A tube that is slightly malpositioned not only causes ventilatory problems, but in some cases it can also jeopardize the surgical repair. In the rare occurrence where OLV is to be continued, it is obvious the best course of action would be to maintain the DLT, even in the ICU setting. The ability to suction and perform regular bronchoscopy through a DLT is critical. However, when OLV is no longer necessary, many patients still require short-term postoperative two-lung ventilation. Not surprisingly, anesthesiologists are reluctant to do this in the presence of a DLT. This is not only due to the expertise needed to manage a DLT, but there is also a widespread belief that DLTs have increased airway resistance versus regular ETTs, making spontaneous respiration even more difficult [57]. A recent study comparing the airflow resistance between multiple tubes, including DLTs, revealed that flow resistance in smaller DLTs is in fact lower than that in corresponding single-lumen ETTs (Figure 19.6) [69]. This study concluded that changing DLTs to single-lumen ETTs on the basis of increased airway resistance is not necessary.

It is also interesting to note that the resistance within Univent tubes was found to be higher than in regular single-lumen tubes, leading to the recommendation that Univent tubes should be replaced at the end of a case. These findings should be emphasized, especially in patients where reintubation is expected to be difficult and losing the airway is a concern. In these clinical scenarios BB technology becomes advantageous. Bronchial blockers can be removed at the termination of a case, leaving a regular ETT to provide normal postoperative ventilation. The risk of losing the airway is therefore diminished, and there is a benefit of having a tube that does not irritate the carina, as in the case of DLTs. However, BBs 11

Univent #7.5 (39) Mallinckrodt 35 Fr (40)

10 9 8 Pd (cm H2O)

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7

Rusch 37 Fr (39) Sheridan 37 Fr (40)

6 5 4

ETT 9.0 ID (40)

3 2 1 0 10

20

30

40

50

60

Flow (l/min)

Figure 19.6. Flow resistances of single-lumen, double-lumen, and Univent tubes. Pressure differential (Pd), an indicator of flow resistance, versus airflow in a subset of the tubes studied. The double-lumen tubes and the Univent tube all have approximately equivalent external circumferences in millimeters, shown in parentheses. These tubes could be used clinically for a small adult patient. Two sizes of single-lumen ETTs are shown for comparison. From [69], with permission.

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Table 19.7: Approach to Airway Tube Exchange Steps

Comments

A. Is tube exchange indicated?

■

B. Assemble equipment.

■ ■ ■ ■ ■ ■ ■ ■ ■

C. Test equipment.

■ ■ ■ ■ ■ ■

D. Ventilate with 100% FiO2 . E. Ensure adequate muscle paralysis.

■

F. Insert laryngoscope.

■

■

■ ■

G. Insert exchange catheter into patient’s DLT (or ETT).

■ ■ ■ ■

H. Remove patient tube. I. Insert new tube over exchange catheter and advance into airway (most difficult step).

■ ■ ■ ■

■ ■

J. Remove tube exchanger.

■

The risk of losing the airway should never be minimized; therefore, indications for tube exchange should always be reviewed. Laryngoscope (GlideScope, WuScope) Endotracheal tubes (at least two sizes) Airway exchange catheter Lubricant Dry gauze or sponge (to provide traction when rotating tube in step I below) Fiberoptic bronchoscope Oxygen insufflation source Suction Assistance for handling equipment Add lubricant liberally to catheter, internal lumen of ETT, and bronchoscope. Test exchanger and bronchoscope in DLT and ETT to confirm easy passage. Remove ETT and exchange catheter connectors for easier passage. Attempt to insufflate oxygen through exchange catheter. Ensure suction is working. Confirm bronchoscope is connected. All airway maneuvers should begin with preoxygenation. A patient that begins coughing during airway manipulation significantly reduces tube exchange success. This provides a better “chin lift,” displaces the tongue very well, and provides a more direct path for the tube exchange. Establish a view of the larynx. Apply suction, if necessary. This usually requires an assistant. Take into consideration depth of insertion by observing markings on exchange catheter (premeasure with an external tube, if necessary). An exchange catheter advanced too deep can cause severe injuries, especially as they are very stiff. Consider using the newest model by Cook that is equipped with a soft, flexible tip. An exchange catheter not advanced deep enough risks losing the airway during the exchange. Care must be taken to keep exchange catheter from moving out with tube. Again, it is important to keep exchange catheter depth constant in order to avoid injury. Care must be taken not to damage the cuff along the patient’s teeth. When the tube touches the larynx, resistance will be felt. Excessive pressure here only makes advancement more difficult and causes injury. Moderate to low pressure should be applied while slowly rotating the tube. This allows the bevel of the ETT to “unhook” itself from the obstruction and then it will advance. If the advancing pressure is too strong, then the distal tip of the ETT will not rotate well. Instead, the tube itself might twist. Use gauze to help grip tube, if necessary. The obstruction is usually visible with laryngoscopy, helping to direct tube rotation. Often, complete 360◦ rotation is necessary to overcome obstruction. Immediately check correct tube placement with bronchoscope, PET CO2 , and auscultation.

are still used infrequently and DLTs remain the standard of care for OLV. Many anesthesiologists therefore elect to remove a DLT at the end of a case and replace it with a regular ETT. If this management approach is to be taken, then safety with airway tube exchange must be emphasized. This can be done with relative safety, but it involves meticulous preplanning and preparation. Tube Exchangers Airway tube exchange is a maneuver burdened with risk. This cannot be overemphasized, as even attempting a tube exchange

is usually based on a known or expected difficult airway. This scenario is common in thoracic surgery, especially in thoracic trauma patients. Preplanning is the key principle that is critical to a successful tube exchange. Table 19.7 presents a suggested approach to airway tube exchanges, using the Cook Airway Exchange Catheter, a commonly available tube exchanger especially designed for DLTs. There are a few clinical “pearls” that can be employed to increase the success rate of tube exchanges. First, it is always important to apply a very generous amount of lubricant to both the exchanger and the internal lumen of the ETT. Second, the use of a rigid fiberoptic laryngoscope (GlideScope or WuScope)

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for assisting in a tube exchange offers many advantages [70]. The view of the larynx is greatly enhanced, and when there is resistance at the larynx to passing a tube over the exchanger, this view easily allows the anesthesiologist to adjust the tube appropriately, increasing the efficiency of success. Third, the tube exchanger size should be chosen carefully. The largest exchanger that fits into the smallest ETT should always be used, if possible. This allows for a smaller gap between the exchanger and the edge of the ETT, which is the main source of resistance when passing the ETT through the larynx. If resistance is encountered, it is almost always secondary to a laryngeal structure (i.e., arytenoids, vocal cords) becoming lodged within this gap. Excess pressure applied at this point only makes the tube more difficult to pass and if excess pressure is applied, the probability of laryngeal injury increases significantly. Success is better achieved by applying continuous moderate pressure at the site of resistance while slightly rotating and advancing the tube. This allows for the bevel of the ETT to pass over the structure that is lodged within its lumen, resulting in a loss of resistance and tube advancement.

c. Increasing FiO2 to 100% d. Adding CPAP to the non-ventilated lung e. Adding 10 cm H2 O of PEEP to the ventilated lung 3. The following are all absolute indications for lung isolation EXCEPT: a. b. c. d. e.

Hemorrhage Thoracoscopy Bronchopleural fistula Lung lavage Video assisted thoracoscopic surgery

4. Below is an endoscopic image of the airway. Which bronchus is the arrow pointing to? a. b. c. d. e.

Right bronchus intermedius Right lower lobe bronchus Left lower lobe bronchus Left mainstem bronchus Right mainstem bronchus

S U M M A RY Lung isolation for thoracic trauma is a difficult procedure that inherently carries plenty of risk. Meticulous preplanning and equipment checking is necessary for smooth delivery of care. Indications for lung isolation must always be reviewed and a plan discussed with the surgical team. Thorough knowledge of lung isolation techniques and bronchial anatomy is essential since patient characteristics often dictate the best technique of choice. When lung isolation is established and positive pressure ventilation is instituted, care should be taken to prevent and treat potential complications. Lung ventilation strategies that further reduce the risk of lung injury should be employed at all times. Intraoperative hypoxemia should always be expected and treated appropriately. Finally, the anesthesiologist must consider multiple factors when planning postoperative management, including method of ventilation, choice of ETT, patient location, and expected duration of intubation.


1. A bronchopleural fistula in the left mainstem bronchus is best managed with: a. b. c. d. e.

Univent tube Bronchial blocker Left double-lumen tube Right double-lumen tube Endobronchial tube

2. A 25 year old patient undergoing video assisted thoracoscopic bullectomy develops mild hypoxemia during onelung ventilation. All of the following are appropriate initial interventions EXCEPT: a. Checking tube position with fiberoptic bronchoscopy b. Adding 5 cm H2 O of PEEP to the ventilated lung

5. The white circle shows the opening of which bronchus? a. b. c. d. e.

Right upper lobe bronchus Right middle lobe bronchus Right lower lobe bronchus Left upper lobe bronchus Left lower lobe bronchus

6. The arrow is pointing to which bronchus? a. b. c. d. e.

Left mainstem bronchus Right mainstem bronchus Right bronchus intermedius Right lower lobe bronchus Right upper lobe bronchus

7. The following statements are all TRUE with respect to double-lumen tubes and bronchial blockers EXCEPT: a. Double-lumen tubes are more difficult to insert in difficult airways b. Both double-lumen tubes and bronchial blockers allow for CPAP to be applied to the non-ventilated lung c. Both double-lumen tubes and bronchial blockers allow for bronchoscopy of the non-ventilated lung

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d. Bronchial blockers can be used for selective lobar isolation e. Bronchial blockers provide a simple method for postoperative ventilation 8. The cuff of a bronchial blocker typically requires how many milliliters of air to provide lung isolation? a. b. c. d. e.

1 3 5 7 9

Cardiac tamponade Endobronchial intubation Air embolism Severe hypovolemia Myocardial infarction

13.

14.

16.

Respiratory rate of 8–12 breaths per minute Tidal volume 8–12 mL/kg PEEP to the dependent lung CPAP to the non-dependent lung FiO2 of 100%

d d b e

12.

15.

17.

18.

19.

ANSWERS

1. 2. 3. 4.

9.

11.

10. Management of one-lung ventilation includes all EXCEPT: a. b. c. d. e.

8.

10.

9. A spontaneously breathing patient with a severe right sided pulmonary contusion and hemothorax is in the emergency room. Severe hypotension occurs immediately following intubation with positive pressure ventilation. The patient has received 3 liters of normal saline and a chest tube that drained only 200 mL of blood. Besides tension pneumothorax, the most likely cause for the hypotension is? a. b. c. d. e.

7.

5. b 6. e 7. c

8. d 9. c 10. b

20.

21.

REFERENCES

1. Thierbach AR, Lipp M. Airway management in trauma patients. Anesthesiol Clin N Am 1999;17(1):63–81. 2. Kingsley CP. Perioperative management of thoracic trauma. Anesthesiol Clin N Am 1999;17(1):183–95. 3. Brodsky JB, Lemmens HJM. Left double-lumen tubes: Clinical experience with 1,170 patients. J Cardiothorac Vasc Anesth 2003;17:289–98. 4. Fouche Y, Tarantino DP. Anesthetic considerations in chest trauma. Chest Surg Clin N Am 1997;7(2):227–38. 5. Caplan RA, Benumof JL, Berry FA, et al. Practice guidelines for management of the difficult airway. A report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology 1993;78(3):597–602. 6. Symbas PN, Justicz AG, Ricketts RR. Rupture of the airways from

22.

23.

24. 25. 26.

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I N T R A O P E R AT I V E O N E - L U N G V E N T I L AT I O N 67. Roscoe A, Kanellakos GW, McRae K, Slinger PD. Pressures exerted by endobronchial devices. Anesth Analg 2007;104: 655–8. 68. Bauer C, Winter C, Hentz JG, Ducrocq X, Steib A, Dupeyron JP. Bronchial blocker compared to double-lumen tube for onelung ventilation during thoracoscopy. Acta Anaesthesiol Scand 2001;45(2):250–4.

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69. Slinger P, Lesiuk L. Flow Resistances of disposable double-lumen, single-lumen, and Univent tubes. J Cardiothorac Vasc Anesth 1998;12(2):142–4. 70. Smith CE, Davenport D, Morscher A. Exchange of a double lumen endobronchial tube using fiber-optic laryngoscopy (WuScope) in a difficult intubation patient. J Clin Anesth 2006;18: 398–9.

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20 B U R N I N J U R I E S ( C R I T I CA L CA R E S EV E R E BU R N I N J U RY )

IN

Charles J. Yowler Objectives 1. Describe the classification system of burn depth. 2. Outline the initial assessment of the severely burned patient. 3. Determine burn size using the Lund–Browder Diagram. 4. Assess the airway and the need for intubation. 5. Determine the fluid requirements for burn resuscitation. 6. Determine the requirement for escharotomy. 7. Describe the potential benefits and complications of early burn excision and grafting.

Modern advances in surgery, anesthesia, and critical care have had a significant impact on the treatment of severe burn injuries [1, 2]. Cohorting burn victims in specialized care burn facilities resulted in clinical research studies that led to reductions in hypovolemic shock, respiratory and renal failure, sepsis, and malnutrition. As a result, the burn size that confers a 50 percent probability of death in patients aged 15–45 years has increased from 50 percent total body surface area (TBSA) in 1950 to 80 percent TBSA in 2000 (Table 20.1). Morbidity and mortality following a major burn injury are related to age of the patient, burn size, and the presence of an inhalation injury [3–5]. The greater the burn size the greater the fluid and heat loss to the environment, both of which contribute to organ hypoperfusion and shock. The inflammatory mediator response also increases with burn size as does the degree of immunosuppression. Bacterial colonization increases with the size of the open wound and, in conjunction with the increase in immunosuppression, results in increased risk of life-threatening burn wound infection. Inhalation injury causes pulmonary dysfunction that is exacerbated by the large fluid resuscitation required following major burn injury. The resultant hypoxia and impaired oxygen delivery to tissue further impair organ function. Advanced age limits the ability of the burn patient to tolerate any organ dysfunction or subsequent infection. Every organ is affected by the hypoperfusion and inflammatory mediator response [6] of the initial injury, and homeostasis does not return until definitive wound closure occurs, which may take weeks for a large burn. The significant metabolic changes that accompany a large burn persist for more than 314

9 months and impair return to normal function. Thus, the patient with severe burns poses unique challenges to the intensivist [7].

PAT H O P H Y S I O L O G Y Burn depth is classified as first, second, or third degree (Table 20.2). First degree burns result from damage to the superficial layers of the epidermis. They are characterized by erythema and pain. No open wound is produced and fluid loss and systemic response is minimal. First degree burns are not considered significant and they are not considered when burn size is calculated for fluid resuscitation. In fact, one of the primary causes of overresuscitation and subsequent fluid overload in burn patients is inclusion of areas of first degree burn in estimating burn size for resuscitation formulas. Areas of first degree burn have to be appreciated and ignored in calculations of burn size for resuscitation. Extension of thermal damage to the dermis results in second degree burns. They may be further classified as superficial or deep second degree burns. Superficial injury results in a very painful wound that is blistered or weeping. The wound is pink and blanches with light pressure. This wound typically heals within 10–20 days with minimal to no scarring if infection is avoided. Nevertheless, areas of superficial second degree burn exceeding 20 percent TSBA may require fluid resuscitation and monitoring.

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BURN INJURIES (CRITICAL CARE

Table 20.1: Percent of Total Body Surface Area (TBSA) Burn for

IN

SEVERE BURN INJURY )

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Table 20.2: Burn Depth and Treatment

an Expected 50 Percent Mortality Age (yr)

Burn

Depth

Treatment

First degree

Epithelium

Lotions, pain control

Superficial second degree

Superficial dermis

Antibiotic ointments, pain control

Deep second degree

Deep dermis

Antibiotic ointments, pain control, and may require excision and grafting

Third degree

To subcutaneous tissue

Will usually require excision and grafting

Burn Size (%)

0–5

70–80

5–20

80–90

30–50

70–80

50–60

50–60

60–70

30–40

>77

20–30

Deep second degree burns extend to the deep dermis. The wounds are drier and are red rather than pink. Blanching is minimal and less pain is noted on compression of the wound. These burns will take more than 20 days to heal and can result in significant hypertrophic scarring. Depending on the burn location, size, and condition of the patient, skin grafting is usually recommended. Coagulation of the entire dermis results in third degree burns. These wounds may be charred or white to deep red. They are insensate to pain, although pressure may be noted with palpation. The skin is leathery in nature, and circumferential third degree burns in extremities may compromise distal blood perfusion. Small third degree burns will heal by the sloughing of skin followed by wound contracture and scarring, but burns of significant size will require excision and grafting. Thermal injury causes release of inflammatory mediators that result in a systemic capillary leak syndrome and loss of fluid and plasma proteins into the interstitial tissue. The edema that follows this fluid leak further impairs tissue perfusion and viability. Thus, the paradox of burn fluid resuscitation: too little fluid causes hypoperfusion of the wound and extension of cellular damage, whereas too much fluid causes excessive tissue edema, which impairs perfusion and also results in extension of injury. The immediate hemodynamic response to a large burn is vasoconstriction and a fall in cardiac output. The cardiac index typically falls by 50 percent within 30 minutes of burn injury and is independent of plasma volume. In large burns, if the fluid loss is not immediately addressed, the combination of hypovolemia and impaired cardiac function will quickly lead to fatal burn shock. Patients with preexisting cardiac dysfunction typically cannot tolerate large burns and pose unique challenges to resuscitation. Thus, elderly patients tolerate large burns poorly. For example, while a burn size of 80 percent TBSA in a patient less than 45 years old has an expected survival of approximately 50 percent, a burn of 30 percent TBSA is lethal to 50 percent of patients at age 70. The capillary leak persists at significant rates for the initial 12–24 hours. Following adequate fluid resuscitation, cardiac function returns to normal by 48 hours after burn injury. By the end of the first burn week, the overall hemodynamic picture has reversed itself and the burn patient is vasodilated with supernormal cardiac output. By postburn day 10, the cardiac output typically plateaus at levels that approach 2.5 times predicted normal values. Cardiac output remains at significantly

elevated levels until the wound is closed and the overall hypermetabolic response persists for 9–12 months. This hypermetabolic response is primarily due to the elevated catecholamine levels that follow burn injury, although elevated cortisol and inflammatory cytokines contribute to the response. The hypermetabolic response of high cardiac output, low systemic vascular resistance, low-grade fever, and elevated white blood cell count mimics the response to infection and makes sepsis difficult to recognize in these patients. It needs to be appreciated that an elderly patient who appears clinically to be doing poorly, but has a “normal” invasive hemodynamic profile following burn injury, may in fact be underresuscitated and require further fluids or inotropic agents. INITIAL ASSESSMENT AND R E S U S C I TAT I O N The initial assessment and resuscitation of patients with lifethreatening burns are based on the principles outlined in the Advanced Trauma Life Support program of the American College of Surgeons. The airway and breathing are assessed and a decision made concerning the need for endotracheal intubation (Table 20.3). Inhalation injury is suspected in any patient exposed to smoke in an enclosed space. However, it should be noted that more than 90 percent of patients with exposure to smoke do not have a significant injury and do not require intubation. The signs of smoke exposure such as soot in the nares or orophaynx, singed facial hair, and carbonaceous cough, are indications that smoke exposure occurred; they are not signs that tracheal intubation is required. Symptoms that suggest a significant injury requiring tracheal intubation include hoarseness, stridor, dyspnea, and tachypnea. A decreased level of consciousness, hypoxia, and elevated blood levels of carbon monoxide are other findings that may require intubation. Laryngeal edema may occur secondary to heat or chemical present in the smoke. Airway edema, if present, will increase for approximately 24 hours because of the chemical irritation and ongoing fluid resuscitation. Thus, early intubation is indicated if hoarseness or stridor is noted on exam. Early intubation is often not difficult and a large endotracheal tube should be placed, if possible, as subsequent bronchoscopy is often required [8]. Carbon monoxide is produced by the combustion of organic material, and carbon monoxide poisoning may accompany smoke exposure. Carbon monoxide binds to both hemoglobin

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YOW L E R

Table 20.3: Indications for Tracheal Intubation

Table 20.4: Carboxyhemoglobin Levels versus Symptoms

Inability to protect airway

Level (%)

Hypoxia

0–10

Stridor/hoarseness

Symptom Minimal symptoms (frequently found in heavy smokers)

Large third degree facial burns

10–20

Nausea, headache

Carboxyhemoglobin >20%

20–30

Drowsiness, weakness

30–40

Confusion, agitation

40–50

Coma, respiratory depression

>50

Death

and the mitochondrial cytochrome oxidase system, resulting in profound impairment of aerobic metabolism. Symptoms are directly related to carboxyhemoglobin (COHgb) concentrations (Table 20.4). Thus, all patients with exposure to smoke in an enclosed space should be placed on a 100 percent nonrebreather mask until an arterial blood gas with carbon monoxide level is obtained. Pulse oximetry is inaccurate in the presence of COHgb because it is interpreted as saturated hemoglobin. As the brain and heart are most sensitive to decreases in oxygen delivery, decreased alertness and evidence of cardiac irritability or ischemia are the earliest signs of carbon monoxide poisoning. In the absence of these signs, COHgb levels of less than 20 percent may be treated with 100 percent mask ventilation with the expectation that concentrations will fall to non-toxic levels (60 years Associated inhalation injury

Secondary predictors

Women aged 30–59 years Development of sepsis and multiple organ failure Limited donor sites Delayed resuscitation Morbid obesity Alcohol and substance abuse Diabetes Neuropsychiatric conditions Associated traumatic injury

Blanding and Stiff [1]; O’Keefe et al. [31]; Sheridan et al. [32]; Aldemir et al. [33]; Wolf et al. [35]; Memmel et al. [37]; Yanagawa et al. [38]; Hawkins et al. [39].

may be evidence of abuse [2]. Signs of abuse such as bruises, whip marks, fractures, and head trauma found currently or in old charts are also abuse indicators [2]. Factors Contributing to Mortality The mortality of the burn patient is greatly influenced by the type of burn, the extent of the burn greater than 40 percent, the patient’s age older than 60 years, and the presence of inhalation injury [1, 31–33]. Elderly patients tend to have a worse outcome due to their higher incidence of comorbidity, atrophic skin with a thinner dermis, and slower epithelial proliferation [1]. Young age has not proved to be a predictor of mortality [32]. In a 2001 study it was found that women between the ages of 30 and 59 years have an increased adjusted risk of death compared with men of the same age [31]. A 2006 study showed an increased risk of death for women of all age groups between the ages of 10 and 70 years [34]. The development of sepsis and multiorgan failure is an indication of a poor outcome independent of the sex or age of the patient [35]. Also, patients with limited donor sites and delayed resuscitation have an increased mortality [35]. Morbidity and mortality of the mother and fetus in a pregnant burn patient is primarily dependent on the size of the burn, followed closely by the presence of an inhalation injury [36]. Pregnancy alone does not adversely affect the outcome of the mother(see Chapter 26) [36]. Most fetuses survive if the mother survives and she does not have any significant complications such as sepsis, hypotension, and hypoxia [36]. Other health factors that contribute to mortality include morbid obesity, alcohol and substance abuse, neuropsychiatric conditions, diabetes, and other associated traumatic injury (Table 21.7) [1, 37–39]. Laboratory Tests The burn patient will require large volumes of fluid and frequent ventilator changes during the perioperative period. Many facilities have utilized specific ordering protocols to account for the

amount of lab tests needed [40]. Preoperatively, it is important to have a recent complete blood count, electrolyte panel, including renal functions, glucose, and lactate level, and an arterial blood gas. Other lab tests can be ordered on an individual case basis. Patients with burn injuries are at risk for significant coagulopathies; therefore, it is also important to check a recent coagulation panel prior to anesthesia [3]. These lab tests can be used as a baseline to adjust the anesthetic management throughout the case. Intravenous Access Establishing vascular access is extremely important prior to excision and grafting procedures (see Chapter 4). In most cases, a minimum of two large-bore peripheral intravenous lines or one peripheral and one central line is necessary [3]. It is often difficult to place intravenous lines in these patients because of the extent of the burn. Central venous trauma lines provide excellent routes for rapid fluid administration and the delivery of vasoactive drugs, with the additional advantage of the placement of central venous or pulmonary artery catheters [3, 41]. Pulmonary artery catheters are not routinely placed because of the risk of infection, but they can be used for a brief period in patients with burn injury and ischemia or valvular heart disease to guide fluid administration [1]. The internal jugular and subclavian veins are most commonly used for catheterization, but femoral vessels can be used if the burn involves the neck [3]. Traditionally, central venous access was guided only by the anatomic landmarks and arterial pulsations [41]. This blind approach assumes that each patient has the same anatomy and that their veins have no thrombosis [41]. An ultrasound probe can be used to aid in the placement of the central venous line [3]. The use of an ultrasound probe decreases the risk of complications, including pneumothorax, arterial puncture, hemothorax, hematoma, and nerve injury (see Chapter 32) [41]. These complications are the most significant in patients with coagulopathies, mechanical ventilation, poor pulmonary function, chronic intravenous use, and soft tissue edema; all of which are usually present in a burn patient [41]. If a central venous line is not possible, then a small-bore peripheral vein can be dilated to a larger gauge by using specially designed kits [3]. In children, if intravenous access can not be achieved in a timely manner, an intraosseous infusion can be used to deliver drugs, fluids, and blood with a low incidence of complications until an intravenous line can be placed [42]. Intravenous lines can be safely placed through a burn site if the usual sterile technique is used. Fluid should be routinely warmed by using high-capacity fluid warmers in the operating room to help in preventing heat loss (see Chapter 29) (Table 21.8) [3]. Premedications Burns are often extremely painful and the patients are often very anxious. The goal of premedication is to provide adequate analgesia and anxiolysis [3]. If a patient does not have a secure airway in place, it is important not to oversedate the patient and risk losing the airway, especially if the patient appears to be a potentially difficult intubation. Patients who present for excision and debridement are often already intubated and sedated. It is important to continue this sedation in the perioperative period.

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ANESTHESIA

Table 21.8: Current Information about Central Intravenous Line Changes in a Burn Patient Infection rates increase with catheters left in situ for more than 10 days. Central line infections occur at a frequency of 5–6 infections per 1,000 catheters. This is twice the CDC recognized infection rate for central line infections. Therefore, the CDC has established separate guidelines for the burn patient. Majority of burn units in the United States change central lines every 72 hr to 7 days, every 72 hr for a line that is placed through burned tissue, and every 7 days for a line placed in a site remote from the burn tissue. No wire changes are performed. Central line infections (and not the burn wound) are the most common source of bacteremia in a burn patient. CDC, Centers for Disease Control and Prevention From Sheridan RL. Mechanical and infectious complications of central venous cannulation in children: Lessons learned from a 10-year experience placing more than 1000 catheters. J Burn Care Res 2006;27(5):713–8.

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patients often lose greater than this amount secondary to thrombocytopenia and other coagulation defects [3]. The best intraoperative fluid replacement includes the use of minimal crystalloid and the replacement of losses with packed red blood cells and fresh-frozen plasma [4]. It is important that the patient is typed and crossed for an appropriate amount of blood products prior to beginning the surgery, and that the products are immediately available at induction. In most cases the patient should be given blood immediately upon entering the operating room. It is very difficult to catch up on fluid replacement once infusion falls behind. After the excision and grafting, the burn patient’s coagulation factors and platelets return to baseline values faster than unburned patients [3]. Studies have shown that the number of infections per patient increase with each unit of blood transfused [15]. The increased number of transfusions is also associated with increased mortality [15]. This study did not include blood products given in the operating room [15]. Currently, it is agreed that outside the operating room, the patient’s blood transfusion should be guided by physiologic need, and that in the operating room, secondary to significant blood loss, the patient’s primary fluid replacement should be with blood [15]. S U R G E RY Topical Wound Care

Preparing Appropriate Blood Products Hemostasis is a critical concern during any burn surgery [4]. Large amounts of blood can be lost rapidly during the excision of the burn; therefore, it is important to have an adequate supply of blood products available prior to the excision [3, 4]. It is difficult to keep up once infusion lags behind blood loss. Documented blood loss and transfusion requirements in patients with greater than 10 percent TBSA burn showed a mean blood loss of 0.3 mL/cm2 surface area excised [3]. An average of 20 mL of blood will need to be transfused for each percent of TBSA burned [3]. Other studies have shown that two to three units of packed red blood cells can be easily lost during skin excision of one hand [4]. In burns greater than 25 percent TBSA the patient can exsanguinate [4]. Many centers use various and multiple techniques to try to limit blood loss during excision, including use of tourniquets, postoperative compression dressings, topical epinephrine, topical thrombin, and subcutaneous infusion of saline and epinephrine [3, 4]. Tourniquets have been found to be the most effective technique [4]. Epinephrine-soaked compresses at a concentration of 1:10,000 have been shown to provide good hemostasis, but their effectiveness at preventing considerable blood loss is questionable [4]. Despite the high levels of catecholamine from the epinephrine-soaked bandages, complications such a dysrhythmia are not common due to the reduced affinity of the β-adrenergic receptor in the burn patient for ligands and decreased second-messenger production [3]. Topical thrombin (1,000 units/mL) helps with hemostasis by forming a clot, but this sheet of clot can prevent graft take and donor healing [4]. Subcutaneous infusion of 0.45 percent saline with diluted epinephrine (1:300,000) to the donor sites also helps with hemostasis [4]. Although the extent of the surgical operation is often intentionally limited in most centers to one volume of blood lost,

Prehospital burn wound care is basic and simple [16]. It requires that the burn be protected from the environment with the application of a clean, dry dressing or sheet [16]. A damp dressing should never be used [16]. The patient should be wrapped in blankets to prevent heat loss during transport [16]. The first step in diminishing the patient’s pain is to cover the wounds to prevent contact with exposed nerve endings [16]. Even though this approach sounds simple, it is often difficult to enact, which is unfortunate because inadequate first aid care is often associated with poorer patient outcomes [16]. Once the extent and depth of the wound is assessed and the wounds are cleaned and debrided, the management phase begins [16]. Each wound should be dressed with the appropriate covering to protect the damaged epithelium, minimize bacterial and fungal colonization, and provide a splinting action to maintain the desired position of function [16]. The dressing should be occlusive to reduce evaporative heat loss and minimize cold stress [16]. The dressing should also provide comfort over the painful wound [16]. First degree wounds are minor with minimal loss of barrier function, and therefore require no dressing and are treated with topical salves to decrease pain and keep the skin moist [16]. Second degree wounds can be treated with daily dressing changes and topical antibiotics. Alternatively, the wounds can be treated with temporary biologic or synthetic coverings to close the wound [16]. Deep second degree and third degree wounds require excision and grafting for sizable burns, and the initial dressing should be aimed at holding bacterial proliferation in check until the initial operation is performed [16]. The timely and effective use of antimicrobials has revolutionized burn care, decreasing the number of invasive wound infections [16]. The topical antibiotics can be divided into two classes: salves and soaks (see Chapter 20). Topical antimicrobial salves used for burn wound care include: silver

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Table 21.9: Topical Antimicrobial Salves and Soaks Application

Medication

Advantages/Disadvantages of Use

Salve

Silver sulfadiazine (Silvadene)

Painless application Broad spectrum efficacy Poor penetration of eschar Painful application Good penetration of eschar Metabolic acidosis Painless application Limited antimicrobial spectrum Painless application Limited antimicrobial spectrum Painless application Limited antimicrobial spectrum Effective at inhibiting most fungal growth Cannot be used with Sulfamylon Effective staphylococcal coverage Expensive

Mafenide acetate (Sulfamylon)

Bacitracin Neomycin Polymyxin B Nystatin (Mycostatin) Mupirocin (Bactroban) Soaks

Silver nitrate (0.5%)

Sodium hypochlorite (0.025%) (Dakin’s solution) Acetic acid (0.25%)

Broad spectrum coverage Poor penetration Can inhibit wound healing Methemoglobinemia Excellent bactericidal activity No adverse effects on wound healing Effective against most organisms Can inhibit epithelialization

Townsend et al. [16]; Ramzy et al. [4].

sulfadiazine (Silvadene), mafenide acetate (Sulfamylon), Bacitracin, Neomycin, Polymyxin B, Nystatin (Mycostatin), and Mupirocin (Bactroban) [4, 16]. Silvadene is advantageous because it is painless upon application and has a broad spectrum of efficacy, but it fails to penetrate the eschar and is therefore not adequate for the treatment of deep partial- and full-thickness burns [4, 16]. In contrast, Sulfamylon is more painful on application, but it is associated with much better penetration through the eschar; however, it is associated with a metabolic acidosis [4, 16]. Bacitracin, Neomycin, and Polymyxin B all have an easy painless application but with a limited antimicrobial spectrum [16]. Mycostatin is effective at inhibiting most fungal growth, but cannot be used in combination with Sulfamylon [16]. Bactroban is very effective in staphylococcal coverage, but is expensive [16]. Antimicrobial soaks include: silver nitrate 0.5 percent, sodium hypochlorite 0.025 percent solution (Dakin’s solution), and acetic acid 0.25 percent [16]. Silver nitrate provides broad-spectrum coverage, but also fails to penetrate and can inhibit wound healing and cause methemoglobinemia [4, 16]. Dakin’s solution provides excellent bactericidal activity, without adverse effects on the wound healing [4, 16]. Acetic acid is effective against most organisms, but can inhibit epithelialization (Table 21.9) [16]. Escharotomies When a deep second or third degree burn wound encompasses the circumference of an extremity, the peripheral circulation

of the limb can be compromised [16]. The generalized edema and the nonyielding eschar can impede venous outflow and eventually affects arterial inflow to the distal beds [16]. This can be diagnosed by the symptoms of increased tingling or limb pain and by checking the capillary refill or using Doppler ultrasound signals of the patient’s blood flow [16]. These extremities will require an escharotomy to release the burn wound eschar [16]. This can be done at the bedside by incising the lateral and medial aspects of the extremity with a scalpel or electrocautery unit [16]. Increased muscle compartment pressures may necessitate a fasciotomy [16]. The most common complications from these procedures include blood loss and the release of anaerobic metabolites, which can cause transient hypotension [16]. Constricting truncal eschars can cause a similar problem, except the effect is decreased ventilation secondary to limited chest wall excursion [16]. The truncal eschar is treated similarly to the extremity eschar [16]. Grafting and Excision Traditionally, the treatment of a burn would include dressing changes and topical antimicrobial agents until the eschar separates, then the granulating wound would be covered with split-thickness skin graft [3, 43]. This process would often take three to five weeks [3, 43]. The patients with severe wounds would often die of sepsis, and if they survived, would have severe contractures and hypertrophic scars [3, 43]. A burn is considered to be a major source of inflammatory mediators, which

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play an important role in maintaining the postburn inflammatory response [43, 44]. The consequent acute-phase reaction – including changes in vascular permeability, alterations in coagulation, impaired gut function, hypermetabolic response, and immune depression – leads to increased mortality and morbidity after a severe burn [44]. The concept of early excision and grafting is derived from a goal of possibly averting these deleterious changes by excising the wound before the response is maximized [43, 44]. Delays in excision and grafting are associated with longer hospitalizations, delayed wound closure, increased rates of invasive wound infection, and sepsis [19, 44]. Early excision within the first 48 hours (assuming that the patient has had sufficient resuscitation), early nutritional support, infection control, biologic wound covering, and modulation of the hypermetabolic response is recommended for optimal burn patient care [3, 43, 44]. Serial excision of the full-thickness burn wound is the current standard of care in many burn centers throughout the world [4]. Operations of excision and grafting are often limited to about 20 percent of TBSA per surgery [3, 4]. With multiple surgical teams and the use of previously described techniques to limit blood loss, larger areas can be excised without increasing the operating time or blood loss [3]. These procedures will be repeated every two days until the burn wound excision is complete [3]. The goal is to perform the entire excision of the burn within ten days of the injury [4]. All of the full-thickness burns should be excised first [4]. This early near-total burn excision has dramatically improved the survival rate in massive burn cases [4]. Facial burns are often treated last, and superficial burns normally heal on their own within two weeks [4]. During the burn wound excision, all dead tissue must be removed [4]. This provides a clean and living wound bed that is necessary to prevent postoperative infection, graft loss, and reoperation [4]. The living tissue will appear as a white, shiny collagen net with punctate bleeding [4]. Burns of less than 30 percent TBSA can be successfully covered with skin autografts [4]. The skin autograft is usually a split-thickness graft that is taken with a powered dermatome from the same patient [4]. These grafts are rarely rejected, provide long-lasting coverage, and provide the best cosmetic result [4]. In burns greater than 30 percent TBSA alternative skin grafts are required for coverage [4]. The excised area can be covered with homografts for temporary skin coverage, but the patient will need to be taken back to the operating room once these grafts are rejected and replaced with autografts [4]. The hope is that during these few weeks, the patient’s donor sites will have healed and can be reused [4].

Alternative Skin Care Management Alternative management for the patient with extensive burns includes artificial skin substitutes [3]. The superiority of the dermal substitutes to conventional skin has never been demonstrated, but the most important potential for these products is their ability to temporarily cover the excised wounds until permanent coverage can be established [19]. These types of dressings provide stable coverage without painful dressing changes, provide a barrier to evaporative losses, and decrease pain in the wounds [16]. These grafts should be applied within 72 hours of the injury, before bacterial colonization of the wound occurs

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[16]. These alternative dressings include Integra, Alloderm, and cultured human keratinocytes [3]. Integra is a bilaminate membrane of chondroitin sulfate. The outer silicone layer closes the wound, and the inner layer establishes a vascular supply [3]. The outer layer is removed after two weeks and replaced with thin autologous skin grafts [3]. The remaining deep layer provides structural support; therefore, only a thin autologous graft is required [3]. This thin graft allows the donor site to be used more frequently for harvesting [3]. Large areas of burn wound can be grafted with this skin substitute [4]. It has an advantage over a homograft because of its lack of transmission of viral infections and avoidance of rejection [4]. The disadvantage of Integra is that it is more expensive than a homograft and lacks the immunologic and metabolic benefits of a living temporary cover [4]. Alloderm, an acellular dermal matrix, is derived from human homografts and is similar to Interga in that it also provides support to a thin skin autograft [3, 4]. Alloderm can be used as a dermal replacement in patients with large burns and limited donor sites [4]. It can also be used as a dermal replacement for wounds extending over the joints to prevent contractures [4]. The experimental use of cultured human keratinocytes was initially promising, but recently they have been found to have poor skin coverage, require weeks to grow, are very expensive, and are associated with long-term skin fragility, recurrent open wounds, and increased rate of burn scar contractures [3, 4]. In burns of greater than 95 percent TBSA, the shortage of donor sites and the absolute need to preserve these small donor sites for later needs make the cultured epithelial autografts necessary for patient survival (Table 21.10) [4]. I N T R AO P E R AT I V E M A N AG E M E N T Monitors and Foley Catheter Monitoring for a major burn excision and grafting should be based on the knowledge of the patient’s medical condition and the extent of the surgery (see Chapter 5) [3]. Vital signs and urine output measurement are considered the standard of care in the resuscitation assessment of the burn patient [45]. Invasive monitoring is reserved for the selected high-risk patient and the patient whose resuscitation is failing [45]. Electrocardiogram monitoring may be done from burned surfaces by using needle electrodes or surgical staples to which an alligator clamp is attached [3]. Standard electrocardiogram pads may be placed under a dependant part of the body to provide a satisfactory electrocardigraphic signal in most patients [3]. Pulse oximetry has been the standard of care in all patients undergoing anesthesia since the early 1990s [46]. It is a valuable, noninvasive optical monitoring technique that is used for the continuous measurement of arterial blood oxygen saturation [46]. Pulse oximetry usually gives reliable readings of the blood oxygen saturation, but there are times when significant limitations on the accuracy and availability of pulse oximetry occur [46]. When peripheral perfusion is poor (as in states of hypovolemia, hypothermia, vasoconstriction, low cardiac output, and low mean arterial pressure) oxygenation readings become unreliable or cease [46]. Sites for pulse oximeter readings are frequently difficult to find in the burn patient [46]. Standard

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Table 21.10: Characteristics of Use for Alternative Skin Care Management Alternative Skin Care Management

Characteristics of Use

Integra

Bilaminate membrane of chondroitin sulfate Outer silicone layer closes wound Inner layer establishes vascular supply Provides support to thin-skin autograft Graft large wound areas Lacks transmission of viral infection Avoidance of rejection Expensive Lacks immunologic and metabolic benefits of living skin

Alloderm

Acellular dermal matrix Provides support to thin-skin autograft Dermal replacement option for large burns/limited donor sites

Cultured human keratinocytes

Poor skin coverage Requires weeks to grow Very expensive Long-term skin fragility Recurrent open wounds Increased burn scar contractures Necessary for total body surface area burns >95% to preserve limited donor sites

MacLennan et al. [3]; Ramzy et al. [4].

sites such as fingers and toes may be affected by the burn or unusable due to tourniquet placement [46]. Alternative sites can be used with a standard pulse oximeter probe if the fingers are too severely burned to be used [3]. These sites include the ear, nose, or tongue [3]. Esophageal reflectance pulse oximetry may offer advantages over the standard transmission oximetry if the skin sites for monitoring are limited [3, 46]. Ultimately, the physician may have to rely on arterial blood gas analysis [46]. Arterial blood pressure should be monitored invasively for any large surgical debridement [3]. Indications for an arterial line include arterial blood sampling, continuous real-time monitoring of moment-to-moment blood pressures, failure to take indirect blood pressure measurements, intentional pharmacologic cardiovascular manipulation, and the assessment of supplementary diagnostic clues [47]. Invasive hemodynamic monitoring is recommended in patients with serious burns who do not respond as expected to fluid resuscitation [3]. This suggests that even if patients have normal vital signs, they can actually be hypovolemic [3]. Urine output and arterial blood pressure cannot be considered sufficient criteria for fluid resuscitation in patients with preexisting cardiopulmonary or renal disorders and may even provide inaccurate information [48]. Pulmonary artery catheterization may be indicated in patients who do not respond to

fluid resuscitation or who have preexisting cardiac disease [3]. The pulmonary artery catheter is used to assess the cardiac output, stroke volume, systemic vascular resistance, and calculation of oxygen transport parameters [48]. Central venous pressure and pulmonary capillary wedge pressure have been used as preload indicators to guide volume therapy [48]. The central venous catheter must often be placed through burned tissue, and the catheters should be removed as soon as possible after the excision and grafting procedure to minimize the risk of local and systemic infection [3]. The indication for extended hemodynamic monitoring is frequently present with a TBSA burn greater than 50 percent [48]. As pulmonary artery catheters are not routinely placed secondary to the increased risk of infection, echocardiography can be used to evaluate ventricular function and estimate central venous and pulmonary artery systolic pressure [1]. A catheter should be placed in the patient’s bladder to evaluate hourly urine output [2, 3]. Even with a severe burn to the genitalia, the catheterization can almost always be performed [2, 3]. The use of silver-impregnated Foley catheters can significantly decrease the rate of urinary tract infection in the burn patient [50]. Thermal Regulation Temperature monitoring is essential for any burn patient undergoing anesthesia because hypothermia is common and often difficult to prevent (see Chapter 29) [3]. The burn patient develops a hypermetabolic state in proportion to the severity of the burn injury [3]. Ambient temperature has an important effect on the metabolic rate of the burn patient [3]. A burn patient with a thermoneutral ambient temperature of 28–32◦ C has a metabolic rate that is 1.5 times greater than in a nonburned control patient [3]. If the burn patient’s ambient temperature is decreased to 22–28◦ C the metabolic rate is increased in proportion to the burn size [3]. Therefore, in the burn unit and the operating room, the patient’s temperature should remain thermoneutral to avoid further increases in the metabolic rate [3]. Hypothermia can also exacerbate coagulopathy and can be potentially devastating during operative debridement of burns [51]. The burn patient is particularly susceptible to hypothermia due to the evaporative heat loss that occurs through their wounds [52]. Temperature regulation can be achieved by having the ambient temperature of the operating room greater than 28◦ C, and having all topical and intravenous fluids warmed to 38◦ C [3, 51, 53]. When possible, the nonoperative sites should be covered, and a forced-air warming device used [3]. If available, over-the-bed warming lamps (radiant heaters) and circulating warm water pads can be used [2, 52, 53]. Ventilation Mechanical ventilation is required for patients with more extensive burns, inhalational injury, or respiratory complications [3]. Patients with lung injury often have a substantial increase in dead-space ventilation, so that end-tidal carbon dioxide may not correlate well with arterial carbon dioxide levels [3]. Therefore, arterial blood gases should be measured frequently [3]. For patients with very abnormal gases, the standard ventilator may be inadequate and the use of the burn unit ventilator may be necessary [3]. The goal of mechanical ventilation is to provide gas

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Table 21.11: ARDS Network Ventilator Protocol Volume cycled assist control ventilation Tidal volume of 6 mL/kg presumed body weight Maximum plateau pressure of 30 cm H2 O PEEP and FiO2 are adjusted in tandem with a PaO2 goal of 55–80 mmHg Inspiratory flow rates are adjusted to keep the inspiratory: expiratory ratio between 1:1 and 1:3 Hough CL, Kallet RH, Ranieri VM, et al. Intrinsic positive end-expiratory pressure in Acute Respiratory Distress Syndrome (ARDS) Network subjects. Crit Care Med 2005;33(3):527–32.

exchange with as little barotrauma as possible (see Chapter 30) [16]. Patients with major burn injury frequently develop ARDS. [54] “Permissive hypercapnia” and the current ARDS Network ventilation protocols can be used to lower ventilatory rates and volumes and to maintain the arterial pH at greater than 7.25, thereby limiting the positive airway pressures delivered by the ventilator [16]. These techniques include high PEEP and lowvolume ventilation [55]. The beneficial effects include avoiding lung tissue damage by reducing shearing forces and avoiding alveolar collapse [55]. The high PEEP is also beneficial in helping to avoid pulmonary edema from the massive fluids given during resuscitation [55]. High FiO2 should be avoided if possible because it can cause lung damage and lead to increased rates of pneumonia (Table 21.11) [55]. In addition to the conventional ventilator, new ventilation techniques have been developed in an attempt to improve oxygenation and decrease barotrauma to the lung [16]. One form of ventilation is high-frequency percussive/oscillatory ventilation [16, 54]. This method alternates standard tidal volumes and respirations with smaller high-frequency respirations [16]. This technique recruits alveoli at lower airway pressures and has a percussive effect that loosens secretions and improves pulmonary toilet [16]. It has been used successfully in many centers for the management of oxygen failure secondary to ARDS and as a method for intraoperative ventilation to allow surgical burn wound excision despite severe ARDS [54]. Patients with pneumonia or ARDS may require frequent endotracheal suctioning, chest physiotherapy, and bronchodilator therapy [3, 16]. Adequate humidification and inhalational therapy including: bronchodilators (Albuterol), nebulized heparin, nebulized acetylcysteine, hypertonic saline, and racemic epinephrine have all proved effective in clearing the tracheobronchial secretions and decreasing bronchospasm [16]. Bronchoscopy may also be needed to clear the secretions [16]. Steroids have not proved beneficial to the patient with inhalational injury, and should not be given unless the patient was steroid dependent prior to the injury or has bronchospasm that is resistant to standard therapy [16]. Pharmacokinetics and Pharmacodynamics of Anesthetics in a Burn Patient The pathophysiologic changes that occur after thermal injury alter the pharmacokinetic parameters such as: absorption, bioavailability, protein binding, volume of distribution, and

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clearance [3]. The extent of these changes depends on the magnitude of injury and the time between the injury and the drug administration [3]. The pharmacokinetic parameters of many drugs will change drastically directly following the injury [56]. The pharmacodynamic changes include the changes in the drug–receptor interaction after the burn and appear to account for many of the clinically important alterations in anesthetic pharmacology [3]. In the hypermetabolic acute phase after the burn injury, organ blood flow is reduced because of hypovolemia and decreased cardiac output, which may affect the dosing requirements of many drugs [1, 3]. Changes in blood flow specifically to the kidneys and liver can affect clearance and elimination [1]. Therefore, drugs administered by routes other than intravenously are likely to show delayed absorption [3]. Plasma albumin concentrations decrease and α-1 acid glycoprotein levels increase [3]. Plasma protein binding of albumin-bound drugs such as benzodiazepines are decreased, resulting in an increase in free fraction and thus a larger volume of distribution of the drug [3]. As most anesthetic drugs are not highly protein-bound and because hemodynamic changes with burns are so marked, the effect of the protein binding on the pharmacologic effects of the anesthetics is minimal [3]. The protein binding of acidic and neutral drugs will decrease and higher amounts of the free fraction will be available, while the basic drugs will exhibit increased protein binding and will probably require an increased dosage to achieve the appropriate pharmacologic effect [56]. After the initial resuscitation phase, cardiac output increases, as does the internal core temperature, which usually increases drug clearance [3, 56]. However, there is wide patient-to-patient variability in renal and hepatic function after the burn, so drug therapy must be tailored to each patient [3]. Induction and Maintenance of Anesthesia General anesthesia with the combination of an opioid, volatile anesthetics, and muscle relaxants is the most widely used technique for burn excision and grafting [3]. The induction agents are chosen based on the hemodynamic stability of the patient [1]. Supplemental opioids are important in burn patients secondary to the intense pain they experience [3]. Burn patients usually require large doses of opioids to remain comfortable even in the absence of movement or surgical procedures [3]. The increased dose requirement of the burn patient, especially during the hypermetabolic state, is thought to be due to the activation of endogenous pathways during the stress response [1]. Also, because they regularly receive opioids as a part of their daily care, they become tolerant to these drugs [3]. The choice of volatile anesthetic does not appear to influence the outcome of the anesthesia for burn surgery. [3] Sevoflurane has the advantage of being an ideal agent for inhaled induction of anesthesia in burn patients with abnormal airways [3]. Isoflurane decreases cardiac output and oxygen consumption; however, the reductions parallel one another so that the oxygen supply to the tissue remains sufficient to meet the demands [3]. Various intravenous agents have been used successfully in burn patients [3]. Ketamine offers the advantage of stable hemodynamics and analgesia [3]. It is beneficial for dressing changes and bedside procedures [1]. Its drawbacks include the tendency

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for dysphoric reactions, which can be decreased with coadministration of benzodiazepines, and the tolerance that develops with repeated use [1, 3]. In a hemodynamically unstable patient, etomidate is a reasonable alternative to ketamine for the induction of anesthesia [3]. Etomidate should not be used for frequent dressing changes due to the possible adrenocortical suppressive effects of the drug [47]. In patients who are adequately resuscitated and not septic, thiopental or propofol may be used [3]. Depolarizing muscle relaxants, including succinylcholine, have led to considerable debate concerning timing and use in burn patients because of the potential for hyperkalemia and cardiac arrest [1, 3]. Burn injury results in denervation of the tissue, which causes the entire skeletal muscle membrane, as opposed to the motor endplate only, to develop acetylcholine receptors [1]. On administration of succinylcholine, an exaggerated number of acetylcholine receptors are depolarized, resulting in a massive efflux of potassium from the cell into the extracellular fluid (see Chapter 9) [1]. The hyperkalemia cannot be prevented by giving a defasciculating dose of nondepolarizer prior to the administration of the succinylcholine [1]. The larger the TBSA of the burn is, the higher the likelihood of a hyperkalemic response [1]. The potassium concentration increases within the first minute after succinylcholine administration, peaks within 5 minutes, and starts to decline by 10 to 15 minutes [1]. The hypersensitivity to the succinylcholine begins 48 hours after the burn, and peaks at 1 to 3 weeks [1]. The hyperkalemic response may persist for up to 2 years [1]. Therefore, succinylcholine is safe for the first 48 hours and is best avoided after that [1]. Nondepolarizing muscle relaxants (NDMRs) are often used during excision and grafting of burn patients. Patients with thermal injury are usually hyposensitive or resistant to the action of NDMRs. [1, 3] This effect may take up to a week to develop and may be observed for as long as 18 months after the burn has healed [3]. A marked resistance to NDMRs occurs when the burn is greater than 30 to 40 percent TBSA [1, 3]. The mechanism appears to be due to the acetylcholine receptor proliferation that occurs under the burn and at the sites distant from the burn injury [3]. This increase in acetylcholine receptors is usually associated with resistance to NDMR and an increased sensitivity to depolarizing muscle relaxants [3]. This resistance to NDMRs implies that the burned patient will require larger than normal doses of NDMR to achieve a desired effect and the duration of action will be shorter than normal [3]. Dose requirements can be increased by up to 250–500 percent [1]. If muscle relaxants are being used, then neuromuscular function should be regularly monitored in the patient [3]. Estimated Blood Loss and Fluid Resuscitation during Excision and Grafting Excisional treatment of burn wounds is usually associated with a large operative blood loss [57]. Neither the surface area to be excised nor the time from the burn accurately predict the magnitude of the operative blood loss, but an excision performed less than 24 hours after the injury usually has less bleeding than one performed 2 to 16 days after the injury [57]. Peak hemorrhage appears to occur on days 5 to 12 [57]. Percent area of third degree burn is associated with greater blood loss, but the percentage of TBSA burned is not [57]. Other operative

Table 21.12: Methods for Estimating Blood Loss During Burn Excision and Grafting Method 1: EBL = 100 to 200 ml per 1% tissue excised Method 2: EBL = (% to be excised) × (loss of area ratio) × (EBV in ml)/100 EBL = estimated blood loss, EBV = estimated blood volume. Loss of area ratio = 8 for children and highly vascular areas. Loss of area ratio = 4 for debridement only and less vascular areas. Blanding and Stiff [1].

variables associated with increased blood loss are surgical time, anesthesia preparatory time, and the initial heart rate recorded in the operating room [57]. Many techniques are often used to try to limit the blood loss during excision and grafting [58]. These techniques include the use of tourniquets, multiple surgical teams working simultaneously to decrease the surgical time, epinephrine- and thrombinsoaked gauze, topical vasoconstrictors, compressive dressings, a cell saver, and continuous intravenous vasopressin infusion [58, 59]. In addition to the difficulty in predicting blood loss, the estimation of blood loss during excision and grafting can also be very difficult to calculate [1]. Estimation of blood loss often requires serial hematocrit readings, the use of formulas, and, most importantly, the constant communication with the surgeon [1]. The first formula that can be used is 100 to 200 mL blood loss per 1 percent tissue excised; however, this does not take into account the circulating blood volume [1]. A more specific formula used is the percent to be excised × loss of area ratio × estimated blood volume (mL)/100, [1] in which the loss of area ratio is 8 for children and highly vascular areas, and 4 for debridement only and less vascular areas (see Tables 21.12–21.15) [1]. Aggressive fluid resuscitation is imperative to improving mortality, especially in the initial phase of treatment and during operative excision and grafting [4]. Furthermore, the volume of the fluid given during resuscitation may not be as important as the timeliness in which it is given [4]. Blood loss is usually replaced with crystalloids, colloids, packed red blood cells, and fresh-frozen plasma [60]. Hemodynamic changes after a burn are significant, and must be managed carefully to optimize intravascular volume, maintain end-organ perfusion, and maximize the oxygen delivery to the tissues [4]. The initial goal of the cardiovascular resuscitation during excision and grafting is to correct and prevent hypovolemia [3]. Intravenous fluid is usually given in proportion to the percent of TBSA burned and is guided by the clinical assessment, vital signs, and urine output [3]. In a patient with normal renal function, the urine output should be at least 0.5 mL · kg−1 · hr−1 in adults and 1 mL · kg−1 · hr−1 in children [16]. Lactated Ringer’s solution is usually the fluid of choice, except in patients younger than two years; they should receive 5 percent dextrose Ringer’s lactate [16]. Adequate resuscitation is reflected by stable vital signs, and a urine output of 1 mL · kg−1 · hr−1 [2]. Changes in the intravenous fluid should be made on a regular basis, at least hourly, based on the patient’s hemodynamic response [16]. The objective of the fluid resuscitation is to replace the

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Table 21.13: Fluid Resuscitation of a Burn Patient Protocol at MetroHealth Medical Center for the First 24 Hours Estimated Fluid Volume and Rates

Crystalloid

Colloid

Thawed Plasma

Adult

1. 4 cc/kg per percent burn for the first 24 hr. 2. Give one-half of the fluid in the first 8 hr postburn. 3. Give the balance over the next 16 hr postburn.

Lactated Ringer’s

1. Burns larger than 40% TBSA 2. Burns requiring >50% over the calculated fluid requirements

1. Burns larger than 40% TBSA and those requiring >50% over the calculated fluid requirement at 12 hr postburn 2. Give TP at a ratio of one unit (about 250 cc) per every liter of LR.

Child

1. Use the Brooke Children’s Formula. 3 cc/kg/TBSA burn + maintenance. 2. Half of the 3 cc/kg per percent burn is given over the first 24 hr (added to maintenance rate). 3. The other half is given over the 16 hr

D5LR

Burns larger than 30% TBSA in patients less than age 5 years

1. Burns larger than 30% TBSA in patients age 15 mL/kg Negative inspiratory force >20 cm H2 O PaO2 >60 mmHg at FiO2 Provide extra runners > Provide extra nursing for blood drawing or screening

4 pRBC 4 FFP 1 6pk platelets 90 MINUTES 4 pRBC 4 FFP

4 FWB

120 MINUTES

PROTOCOL TERMINATED WHEN NO LONGER NEEDED

Figure 22.2. Example of massive transfusion protocol. A whole-blood drive could be called if the attending surgeon or anesthesiologist decided this was appropriate. Injury patterns of two limbs plus a body cavity were an indicator that whole blood would probably be needed as was ongoing transfusion of greater than 20 units of packed cells, 20 units of plasma, and other components. pRBC, packed red blood cells; FWB, fresh whole blood; FFP, fresh-frozen plasma; cryoppt, cryoprecipitate; RTD, return to duty; DCCS, damage control casualty station; CSH, Combat Surgical Hospital.

L AT E

This includes anesthesia for relook and delayed procedures. Anesthesia in this situation will depend on the patient’s overall condition. A “relook” for continued bleeding is likely to be similar to the acute interventions outlined above and commonly will involve intensive care patients where the surgery will be a necessary part of their ongoing management. In contrast, an anesthetic for delayed primary suture in a single-limb injury in

a well-resuscitated patient several days postinjury is more likely to be similar to a straightforward day case anesthetic. Planning Anesthesia Casualties injured by modern munitions containing preformed fragments are likely to have multiple penetrating injuries to different body areas [19] and may need frequent repositioning

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Table 22.1: General Principles of Emergency Anesthesia∗ 1. Perform preoperative assessment of patients. This may be very brief and amount to simple triage. 2. Undertake appropriate resuscitation. Appropriate may mean “hypotensive” depending on the situation and type of injury. 3. Explain to the patient what is happening and what is planned and ask for their consent. This will often be done via a translator in NGO/IGO work and consent may involve relatives or societal elders. 4. Check anesthetic equipment and drugs, including the availability of suction apparatus and the ability to tilt the operating table or stretcher. 5. Preoxygenate the patient where possible if oxygen is available, but remember it may need to be rationed. Oxygen sources include cylinders and concentrators. 6. Confirm the plan with the anesthetic assistant. When working with NGOs the training of operating theater helpers may have to be brief and to the point. 7. Perform airway protection for the patient with endotracheal intubation (or a surgical airway) if indicated and if possible. In general, battlefield trauma casualties should be treated as having full stomachs and being at risk for aspiration. 8. Monitor the patient during anesthesia and surgery. The ideal situation is a trained and alert anesthetist working with reliable electronic monitors. For field work the anesthetist must also be trained and experienced in monitoring by physical signs only and in using manual monitoring such as stethoscope and sphygmomanometer. 9. Agree on realistic and appropriate surgical goals. 10. Safe recovery of the patient. This may have to be in the operating theater. In the absence of ITU facilities or postoperative ventilation patients need to be able to breathe for themselves soon after operation. ∗ On

deployment, be aware of the current military situation and any constraints this imposes on clinical care. NGO, nongovernmental organization; IGO, intergovernmental organization; ITU, intensive care unit. From: Cantelo R, Mahoney PF. An introduction to field anaesthesia. Curr Anaesth Crit Care 2003;14:126–30.

during surgery [20]. Fragments and bullets cross body cavities and regions and therefore the theater team must be prepared for the surgeon to convert an abdominal operation into a thoracic one and vice versa. What Type of Anesthesia Can Be Provided? The type of anesthesia provided depends on a number of factors and includes: 1. The training and background of the anesthesia providers 2. The facilities and personnel for patient preparation, recovery, and postoperative care 3. A relatively secure environment to work in. The definition of “relatively secure” is broad and can be interpreted as anything from good operating theater climate

control and rest facilities to no direct threat toward the operating team at that time. 4. Infrastructure. This includes electricity, water, shelter, laboratory support, and availability of blood. Most elements can be worked around if absent. Examples are generators instead of main electricity, hand ventilation instead of mechanical ventilators, head torches if light sources are unreliable, walking blood donors if there is no banked blood supply, and stored water if there is no running water supply. The lack of resources imposes restrictions on how anesthesia and surgery can be achieved and influences the anesthetic technique used for a particular operation. Anesthetic Techniques Field anesthetic techniques can be divided into local, regional, general, and combinations of all of these. General may be a single agent such as ketamine, or a combination of intravenous and inhalational agents. What Techniques Have Been Described? If modern agents and equipment with quality monitoring and inbuilt safety devices are available they should be used. Modularized operating theatres are likely to provide this. Deviation from this will be dictated by circumstance. General Anesthesia Using Volatile Agents Standard hospital-based anesthetic machines in the UK rely on supplies of compressed medical gases for operation. In the field environment medical gas supplies cannot be guaranteed, hence the use of drawover techniques [21] with air as the carrier gas and oxygen supplemented from concentrators or cylinders. The use of compressors and oxygen concentrators has simplified the provision of compressed gas supply. The “Epstein and Mackintosh of Oxford ether inhaler (EMO)” and ether are widely used in developing countries. Most Western anesthetists have little experience with ether, the EMO is relatively bulky, and use of ether is hazardous in the military environment [22]. At time of writing, the British military deploy with the Penlon Triservice Anaesthetic (TSA) apparatus [23]. The U.S. military deploys with the Draeger Narkomed M for use in field hospitals, and a drawover vaporizer for use in the more mobile forward surgical teams. Other systems have also been designed for field use and are suitable for the military [24], for aid agencies, or in developing countries. The TSA apparatus can be used as a simple drawover system with spontaneous ventilation, as a manually controlled intermittent positive pressure ventilation system, or with a mechanical ventilator. Mechanical ventilation can be in drawover or pushover modes. The apparatus is compact and robust and it has been used successfully in many operational environments [20, 25, 26]. The original description by Houghton included using two Oxford Miniature Vaporisers in series. One Oxford Vaporiser contained halothane and the other trichloroethylene. Trichloroethylene provided analgesia. The system can be further simplified to one vaporizer and resuscitation bag for forward use or in disaster settings. Disadvantages of the Oxford Miniature Vaporiser include lack of temperature compensation, the small volume of anesthetic

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agent it contains, and the potential risk of contaminating the circuit with liquid volatile agents should the vaporizer be tipped over, although this should not happen if the vaporizer is correctly secured. The apparatus has been used successfully with enflurane, isoflurane, and halothane. Current UK military practice usually involves air (supplemented with oxygen) as the carrier gas and isoflurane as the volatile agent. At time of writing, UK forces use the CompPAC ventilator [27]. If working with aid agencies, anesthetists can expect to have to use older, less expensive agents. Where inhalational agents are neither available nor appropriate, intravenous anesthesia is an alternative. Total Intravenous Anesthesia (TIVA)

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propofol/remifentanil infusion is also suitable for field use with ventilated patients. Potential disadvantages for infusion-pump-based IV anesthesia include servicing and maintenance of the pumps and batteries in the field and supply of the necessary consumables and disposables from the logistic chain. In the absence of intravenous infusion pumps or power supplies, intravenous anesthetics and anesthetic/analgesic mixtures can be injected into bags of compatible intravenous fluid and titrated to effect (see Figure 22.3, see also color plate after p. 294).

Example of Anesthesia Recipe An infusion of 4 mg of propofol, 2.5 mg of ketamine, and 2.5 µg of fentanyl per milliliter of solution is easily administered. To mix the solution, 40 mL of 1 percent propofol, 250 µg (5 mL of 50 µg/mL) of fentanyl, and 250 mg of ketamine (5 mL if using 50 mg/mL concentration) are added to 50 mL of saline (see Figure 22.4, see also color plate after p. 294). Using a standard 20 drop/mL drip set and assuming an 80-kg patient, one drop per second equates to a propofol infusion rate of 150 µg · kg−1 · min−1 (or 9 mg · kg−1 · hr−1 ). One drop every three seconds equates to a propofol infusion rate of 50 µg · kg−1 · min−1 (or 3 mg · kg−1 · hr−1 ). For most soldiers, these rates provide good starting points for a range of anesthetics, and the infusion rates are easily titrated as needed, based on the patient’s response (or lack thereof) to ongoing surgical stimuli. This infusion can be terminated at the end of the case, or continued in the intensive care unit at lower rates to provide sedation and analgesia.

The use of intravenous anesthesia in war was criticized by Halford [28], although contemporaneous reports gave advice on how IV anesthesia should be used appropriately [29, 30] and this was the subject of an article in 1995 [31]. A number of different intravenous techniques have been described by UK military anesthetists. These range from ketamine increments [26] to mixtures of agents given alone or in combination with a volatile anesthetic. Restall et al. [32] described using a maintenance mixture of ketamine, midazolam, and vecuronium delivered by a syringe pump for intubated patients whose lungs were being ventilated with air. This was felt to be an appropriate technique for the initial anesthetic for battle casualties. A later study found the ketamine/midazolam combination to be comparable to one based on propofol and alfentanil [33] and use of a propofol/ alfentanil combination was reported in the 1990–1991 Gulf War [34]. A subsequent technique for patients who could be allowed to breathe spontaneously (e.g., fasted casualties undergoing a delayed primary suture of a wound) involved a background infusion of ketamine, midazolam, and alfentanil supplementing the inhalation of isoflurane in oxygen enriched air [35]. A

This mixture (4 mg of propofol, 2.5 mg of ketamine, and 2.5 µg of fentanyl per milliliter of mixture) contains a fairly high dose of ketamine relative to fentanyl. Although the

Figure 22.3. An Iraqi patient undergoes surgery on a traumatically amputated thigh while spontaneously ventilating. He did not have any regional anesthetic and is receiving a titrated mixture of propofol, ketamine, and fentanyl mixed in one bag. Photo courtesy of C. McFarland.

Figure 22.4. Equipment required for the Field TIVA technique described in the box. The medications are propofol, fentanyl, and ketamine. The drip set is 20 drops per milliliter. No anesthesia machine, infusion pumps, batteries, or electricity are required to deliver an anesthetic in this manner, resulting in minimal logistical impact. Photo courtesy of C. McFarland.

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pharmacokinetics and pharmacodynamics of propofol and opioids given concurrently has been elucidated by several studies [36–38], and the use of propofol-ketamine combinations has also been described [39], there are currently no studies that model the effect of infusing these three agents simultaneously. Our impression is that, as the propofol is rapidly redistributed from its effect site and spontaneous ventilation returns quickly, the pharmacokinetics of ketamine and fentanyl results in a slow return to full arousal. The clinical result is a patient who is sedated and comfortable, but who maintains his own airway. This is of obvious benefit, especially when nursing care is at a premium in the combat hospital or field environment. In a patient in whom postoperative sedation is to be minimized, that is, the patient is expected to perform self-care, it may be desirable to omit ketamine from the mixture. Ketamine can still be used in more limited amounts as an analgesic adjunct during or after the operation in doses of 0.1–0.25 mg/kg as needed. This takes advantage of the opioid-sparing effects of ketamine, without substantially risking its adverse psychotropic effects [40–45]. Another modification of the TIVA mixture involves substituting an equipotent amount of sufentanil for fentanyl. The faster elimination of sufentanil allows for a more speedy return to full arousal [38], although the time to first postoperative opioid requirement is expected to be reduced as well. Ketamine Ketamine has the disadvantage that there is limited experience of it in routine UK practice. The anesthetic technique that anesthetists can best use under pressure is usually the technique they are most familiar with. Ketamine has a large number of pharmacologic effects and clinical uses [46, 47]. In addition to the combinations just described, ketamine can be used as a sole anesthetic agent either by intravenous or intramuscular injection [48]. Although the patient’s upper airway reflexes remain more competent with ketamine than with other sedative agents [49], they are not guaranteed [50], and airway obstruction, apnea, and pulmonary aspiration can occur. Where practical, patients receiving ketamine deserve the same degree of preoperative preparation and intraoperative and postoperative care as those receiving other agents. Ketamine increases salivary secretions and use of a prophylactic antisialogogue such as atropine or glycopyrrolate is helpful. Ketamine’s sympathomimetic effect usually causes an increase in blood pressure and heart rate and it is very useful in hemodynamically compromised patients [51], although blood pressure in these patients may fall on induction of anesthesia with ketamine. Ketamine is associated with emergence phenomena, but the incidence of this is decreased by benzodiazepines. Both the emergence phenomena and heavy use of benzodiazepines prolong recovery time, which must be considered if early evacuation of the casualty is going to take place. The reported side effects of ketamine have for decades tempered enthusiasm for its use. However, there has been a resurgence of interest in the drug, and it has been the subject of a number of studies that have refined our understanding of its effects. The results are summarized in Table 22.2. Interestingly, ketamine has been shown to improve mood and possibly allow earlier return of cognitive function when used with propofol [52].

Table 22.2: Updated Effects of Ketamine Previously Reported Side Effect of Ketamine

Results of Most Current Research

High rate of psychotomimetic effects

When combined with premedication, incidence occurs between 0 and 2%. Psychotomimetic effects are related to plasma concentration of ketamine [65], which are reduced via S(+)-ketamine and advances in TIVA and TCI.

Increased ICP

When subjects are controlled for arterial carbon dioxide concentrations, there is no direct or indirect increase in ICP [66, 67].

Cardiovascular depression and stimulation

There is no human in vivo evidence of myocardial depression. Myocardial depression was only seen in canine in vitro myocardial tissue at extreme (nonclinical) levels of ketamine [68]. In vitro, ketamine has been found to be the least potent cardiodepressant of all IV anesthetics [69]. Cardiac stimulation is consistently attenuated with benzodiazepine premedication [70].

Increased salivary and tracheobronchial secretions

Antisialogogues, especially glycopyrrolate, are efficient at attenuating an increase in secretions.

Courtesy of Grathwohl K. (This table was modified with permission from Dr. Kurt Grathwohl’s notes in the syllabus of the conference “Taking TIVA into the 21st Century – Applications for Clinical Practice and Disaster Medicine,” March 9–10, 2006.) ICP, intracranial pressure; TIVA, total intravenous anesthesia; TCI, target controlled infusion.

The major benefits of ketamine are outlined in Table 22.3. It is worth noting that S(+)-ketamine is thought to have lower incidence of side effects (psychotropic effects, salivation) and more rapid metabolism, yet it produces more intense analgesia at an equimolar dose in comparison with R(–)-ketamine [53]. Although we have no experience with S(+)-ketamine, we postulate that these characteristics would allow it to shoulder a greater proportion of the analgesic burden than racemic ketamine either as a component of TIVA, or as a stand-alone analgesic agent.

Regional Anesthesia A number of authors have described using regional anesthetic techniques in field conditions. These vary from simple infiltration of local anesthetics to nerve conduction blocks and spinal anesthesia [54, 55].

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Table 22.3: Major Benefits of Ketamine Category

Beneficial Effects

Pulmonary System

1. Protective airway reflexes more likely to be preserved than with other IV anesthetics 2. Maintains respiratory function 3. Bronchodilation 4. Treatment and induction agent for status asthmaticus 5. Maintains the hypoxic pulmonary vasoconstriction reflex [71] 6. Decreases patient supplemental oxygen requirements

Cardiovascular System

1. Confers hemodynamic stability to hypotensive induction agents (e.g., propofol, opioids) [72, 73] 2. Protects against redistribution hypothermia [74] (thus reducing coagulopathy, delayed wound healing, and increased O2 consumption)

Neurologic System

1. Neuroprotective [75] 2. Potent analgesic when used alone, and increases analgesic effects of opioids when used in combination 3. Attenuates opioid tolerance [76]

Circumstantial Uses

1. 2. 3. 4. 5.

Anti-inflammatory [77] Useful in septic shock [78] Useful in pericardial tamponade Useful in asthmatics Multiple routes of administration: IV, IM, intraosseously, nasally, rectally, and orally 6. No issue of waste gases, thus negating need for scavenger systems 7. No risk of malignant hyperthermia

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ing avoiding a potentially difficult airway, avoiding risk of aspiration, decreased sore throat, decreased postoperative nausea, decreased postoperative pain, and potentially decreased blood loss. Combinations of regional anesthetic techniques supplemented with intravenous ketamine or other agents can be very useful [59]. When regional anesthesia is used to supplement general anesthesia, the general anesthetic requirements are decreased. Disadvantages include a variable failure rate, and concerns about hygiene and introducing infection when performing the technique. Complications are predictable and include: ■ ■

Hypotension in underestimated hypovolemia. Nerve injury – usually sensory changes that resolve – occurs at rates of 0.1 percent, and life-threatening complications are very rare.

Perhaps the greatest barriers to using regional anesthesia in the combat setting are systemic barriers. For example, it takes additional time to prepare before surgery and requires additional equipment and the technique may be discouraged by surgeons not familiar with its value. Casualties injured by modern munitions containing preformed fragments are likely to have multiple penetrating injuries to different body areas [19] and to need repositioning during surgery. Regional anesthesia has only limited use as a sole technique in these patients but may have a major role to play in postoperative care and evacuation (see Figure 22.5, see also color plate after p. 294). In the patient with a traumatized extremity, one must be careful to monitor for the development of compartmental syndrome. Diagnosis of compartmental syndrome in the absence of compartment pressure monitoring depends on evaluation of pulses, paresthesias, paralysis, pallor, pain on passive range of motion, and extreme pain out of proportion to the injury. Some surgeons have been hesitant to allow peripheral nerve catheters to be placed, for fear of masking the painful symptoms of this

Courtesy of Grathwohl K. (This table was modified with permission from Kurt Grathwohl’s notes in the syllabus of the conference “Taking TIVA into the 21st Century – Applications for Clinical Practice and Disaster Medicine,” March 9–10, 2006.)

Neuraxial blockade proved beneficial during World War II, when Samuel Liebermann reported a decrease in mortality from 46 percent to 12.5 percent after switching from volatile agent anesthesia to continuous spinal anesthesia for abdominal wounds [56]. Military anesthetists used peripheral nerve blocks extensively in the Vietnam Conflict, as reported by Gale Thompson [57, 58]. Jowitt and Knight found caudal epidurals to be successful for pain relief in patients with trench foot during the 1982 Falklands War [26]. The advantages of a pure regional anesthetic are that the patient is spared a general anesthetic and is awake and protecting his own airway. This is particularly advantageous in a combat setting, where nursing care may be limited. Other advantages are familiar to the nonmilitary practitioner, includ-

Figure 22.5. A soldier who suffered bilateral traumatic amputations of the upper extremities above the elbow during Operation Iraqi Freedom has his pain managed with bilateral infraclavicular brachial plexus catheters. Photo courtesy of Army Regional Anesthesia & Pain Management Initiative.

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Figure 22.6. Equipment needed for single injection or continuous regional techniques. The StimuQuik™ insulated peripheral nerve block needle by Arrow®, the Contiplex® Tuohy Continuous Nerve Block Set by B-Braun, and the PainPump2® by Stryker® are among the equipment shown. Photo courtesy of C. McFarland.

complication. Note that a patient who describes their pain as being “10 out of 10” despite optimal medical pain management already has extreme pain that deserves to be treated, whether a fasciotomy is indicated or not. If an extremity is at risk for compartmental syndrome, it would be prudent to provide an analgesic infusion of a dilute local anesthetic solution rather than a fully anesthetic block with larger volumes of more concentrated solutions. For a number of the severe limb injuries resulting from IED blasts in Iraq, using a regional anesthetic technique was the only satisfactory way to achieve pain control. At the 10th Combat Support Hospital 2006, the main techniques used (by Lt. Col. Gehrke, U.S. Army) were popliteal nerve blocks and epidural blockade using tunneled catheters placed aseptically in the operating room. A smaller number of supra- and infraclavicular brachial plexus catheters and sciatic nerve catheters were also used. Local anesthesia (0.2% Ropivacaine) was delivered by using the Stryker PainPump2® (Stryker Instruments, Kalamazoo, Michigan) a refillable disposable infusion pump (Figure 22.6, see also color plate after p. 294). Ultrasound-guided placement of supraclavicular continuous nerve block in the United States in a combat casualty has been described [60]. In Mosul, Iraq, in 2006, a GE Voluson i ultrasound machine (www.gehealthcare.com) was used for more than seventy-five successful extremity blocks, demonstrating its utility in the combat theater move over (See Figure 22.7, see also color plate after p. 294.) [81]. IED casualties usually had other injuries from multiple penetrating fragments or suffered from burn injuries. Analgesia for these patients was achieved with an intravenous opiate patientcontrolled analgesia (PCA; usually morphine or fentanyl) with the Sorenson Ambit PCA pump. Patients with regional techniques in situ were tracked through the Casevac system using a regional anesthesia tracking system that notified anesthesia providers registered with the tracking system each time a patient was moved to a new location.

Figure 22.7. Dr. Malchow uses a portable ultrasound to facilitate femoral nerve block in a patient with external fixation of his femur. Photo courtesy of R. Malchow.

Regional Anesthesia in Combat Casualties and Thromboprophylaxis Postoperative immobile patients are at risk for developing deep vein thrombosis and pulmonary embolism. Patients undergoing prolonged evacuation are also at risk. Postoperative combat casualties at the 10th Combat Support Hospital received thromboprophylaxis. The choice of regional technique and of thromboprophylaxis medication used was a balance of risk and benefit based on American Society of Regional Anaesthesia (ASRA) guidelines, although these guidelines do not address the particular issues posed by multiply injured combat casualties [61]. Accepting that patients being evacuated would not be as easy to monitor and assess for complications in the back of an aircraft compared with a standard postoperative care unit, the aim was to provide optimum analgesia and thromboprophylaxis but minimize potential bleeding complications from continuous catheter sites. The 2006 protocol was that patients with an epidural catheter in situ received unfractionated heparin. At the time of writing, there has been no reported case of an epidural hematoma in the combat theater when similar guidelines are in place. Some surgeons felt that thromboprophylaxis with lowmolecular-weight heparin is more reliable than with unfractionated heparin and were reluctant to see epidurals placed in their patients if this then required them to use unfractionated heparin. Given the reports of deep vein thrombosis and pulmonary embolism in evacuated combat casualties [62], and the absence of epidural hematoma reports, the anesthetist and surgeon may decide to place an epidural and use low-molecularweight heparin. If not, they may decide to place an epidural and use standard heparin, or avoid the epidural altogether. Patients with peripheral nerve catheters in situ received low-molecularweight heparin. The current ASRA guidelines do not make specific recommendations concerning peripheral blocks and thromboprophylaxis [82]. Should bleeding occur at a peripheral block site, it may be compressible, depending on which specific block was

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Table 22.4: Pros and Cons of Techniques for Military Anesthesia Technique

Pros

Cons

General anesthesia with volatile gases

Familiar concept to anesthetists Reliable

Large logistical footprint (weight and space) Many anesthetists unpracticed on drawover/pushover vaporizers Highest requirement for supplemental oxygen Risks malignant hyperthermia

Total intravenous anesthesia

Versatile (analgesia, sedation, or intraoperative anesthetic) Adaptable to use many different drugs Small logistical footprint Does not require electrical supply Lower risk of redistribution hypothermia if ketamine included

Lack of familiarity to many anesthetists Dependent on IV access

Regional anesthesia

Dramatic pain control without altering consciousness Lowest requirement for supplemental oxygen Lowest acuity of postoperative care Small logistical footprint Attenuates pain-induced stress response Can be used to supplement other techniques

Failure rate related to the expertise of anesthetist Neuraxial techniques risk hypotension and redistributive hypothermia Concern for spinal hematoma if anticoagulated Cannot be used as sole technique in many multiply injured patients Can be time-consuming

Ketamine as sole anesthetic

Suitable for analgesia during tactical field care Can provide a total anesthetic (hypnosis, analgesia, amnesia, muscle relaxation) Supports hemodynamics Airway tone and spontaneous ventilation maintained better than other systemic anesthetics Versatile adjunct to other techniques

Associated with psychotomimetic effects if not used with other sedatives Salivation/lacrimation

performed. Buckenmaier et al. [63] have recently been investigating this issue and made recommendations.

evidence to ensure that the best possible care can be delivered to casualties whatever the circumstances.

Monitoring

AU T H O R S ’ N O T E

Current UK medical doctrine aims to provide standards of care as close to peacetime National Health Service standards as possible (allowing for battlefield conditions) and delivered within defined clinical timelines. While recent UK military operations have included modern electronic monitors (such as the Datex AS/3 and the Propaq) the anesthetist must be able to go back to more basic clinical methods as described earlier. Nongovernmental organization deployments may not include monitors at all [64]. C O N C LU S I O N S Anesthesia for the multiply injured casualty is challenging. Anesthesia for the same casualty in a deployed environment is even more so. The practitioner working in this environment needs to understand the constraints imposed and be able to provide anesthesia by drawing on a variety of different techniques (Table 22.4). This does not mean that the standard of care given to the casualty is reduced. Military practice is constantly looking at new technologies, new techniques, and new

The views expressed in this chapter are those of the authors based on operational experience and do not necessarily reflect the views of the UK or U.S. military. AC K N O W L E D G M E N T S We thank Dr. K Grathwohl for permission to use his material for the ketamine tables. Dr. Grathwohl is a Lieutenant Colonel in the U.S. Army, an anesthesiologist at Brooke Army Medical Center in San Antonio, Texas, and an Associate Professor at the Uniformed Services University for the Health Sciences in Bethesda, Maryland.


1. What problems can civilian contractors present to military anesthetists? a. Hypertension

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Angina Diabetes Asthma All of the above

2. True or False. Military medical practitioners always expect protection under the Geneva Conventions? a. True b. False 3. UK Battlefield Trauma Life Support is teaching “staged care.” What are the stages? a. b. c. d. e.

Care under fire Tactical field care Field resuscitation Advanced resuscitation. All of the above

4. When receiving casualties who have been treated in another health care system what should you do? a. Immediate tracheal intubation b. Administer broad spectrum antibiotic c. Perform a thorough examination and investigation in case injuries have been missed. d. Diagnostic peritoneal lavage e. Administer high-flow oxygen by mask 5. Identify the correct statements concerning military trauma. a. The trauma team needs to be briefed with available prehospital information b. An organized team leader helps the team perform effectively c. Key personnel include translators for civilian patients and administrators for patient tracking and documentation d. Trauma team activation is based on a combination of history, vital signs, and mechanism of injuries e. All of the above 6. Hypotensive resuscitation (target systolic blood pressure, 80–90 mmHg) is suitable for all casualties. a. True b. False 7. Combat casualties with peripheral nerve catheters should receive thromboprophylaxis. a. True b. False 8. What type of injury patterns occur with IEDs? a. Burns b. Multisystem injuries c. Multicavity injuries

d. Penetrating and/or blunt trauma e. All of the above patterns can occur with IEDs depending on type of device and where the victims were in relation to the explosion. 9. Identify the correct statement regarding ketamine. a. Guarantees preservation of airway reflexes b. Can be given nasally, orally, intravenously, intramuscularly, and rectally c. Does not require the same degree of intraoperative and postoperative care as other anesthetics d. Decreases salivary secretions e. Usually causes a decrease in blood pressure 10. Regarding the use of regional anesthesia, identify the correct statement. a. Does not allow the patient to maintain their own airway. b. Cannot mask the symptoms and signs of compartmental syndrome. c. Requires additional time and equipment for its successful use (e.g., peripheral nerve stimulator and/or ultrasound). d. Life-threatening complications are common. e. Nerve injury occurs in 5 percent of cases.

ANSWERS

1. e. Recent experience in Iraq and Afghanistan has been that some contractors have deployed with undeclared chronic health problems that complicate anesthesia. 2. b. Recent experience is that, unfortunately, no. Medics must act within the Geneva Conventions but must also be aware that, in current conflicts, the enemy is not respecting the Conventions. 3. e 4. c 5. e 6. b. This is still an area of debate and investigation. Patients with head injury or who have suffered blast injury may not be suitable for hypotensive resuscitation. 7. a. The question to be answered is really which regimen of thromboprophylaxis is most appropriate. 8. e 9. b 10. c

REFERENCES

1. Bellamy RF. The nature of combat injuries and the role of ATLS in their management. In Combat Casualty Care Guidelines: Operation Desert Storm. Washington DC: Office of the Surgeon General, 1991. 2. Perrin P. Protecting the victims of armed conflicts. In Perrin P (ed). Handbook on War and Public Health. Geneva: International Committee of the Red Cross, 1996, pp 377– 403.

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FIELD ANESTHESIA 3. Ignatieff M. The Warrior’s Honor: Ethnic War and the Modern Conscience. London: Chatto & Windus, 1998, p 129. 4. Battlefield Advanced Trauma Life Support (BATLS) 2005. Joint Service Publication 570. Open publication as: Supplements to Journal of the Royal Army Medical Corps June 2006;152(2), September 2006;152(3) and December 2006; 152(4). 5. Butler FK, Hagmann J, Butler EG. Tactical combat care in special operations. Mil Med 1996;161(suppl 1). 6. Hayward-Karlsson J JS, Kerr A, Schmidt H. Hospitals for War Wounded. Geneva: International Committee of the Red Cross, 1998, p 88. 7. Botha A, Loosemore T, eds. Definitive Surgical Trauma Skills. London:The Royal College of Surgeons of England, 2002, pp 10–12. 8. Hodgetts T, Mahoney PF, Mozumder A, McLennan J. Care of civilians during military operations. Int J Disaster Med 2005;3:3–24. 9. Hodgetts TJ, Mahoney PF, Russell MQ, Byers M. ABC to ABC: Redefining the military trauma paradigm. Emerg Med J 2006;23:745–6. 10. Bellamy RF. Combat trauma overview. In Zajtchuk R, Grande CM, ed. Textbook of Military Medicine. Part 4: Surgical Combat Casualty Care: Anaesthesia and perioperative Care of the Combat Casualty. Falls Church, VA: Office of the Surgeon General, U.S. Army, 1995, pp 1–42. 11. Barkana et al. Prehospital stabilisation of the cervical spine for penetrating injuries of the neck – Is it necessary?. Injury 2000;31(5):305–9. 12. Criswell JC, Parr MJA, Nolan JP. Emergency airway management in patients with cervical spine injury. Anesthesia 1994;49: 900–3. 13. Greaves I, Porter K, Revell MP. Fluid resuscitation in prehospital trauma care: A consensus view. J R Coll Surg Edin 2002;47(2):451–7. 14. Pepe PE. Shock in polytrauma. BMJ 2003;327:119–20. 15. Wiggers CJ. Physiology of Shock. New York: Common Wealth Fund, 1950, p 121–46. 15a. Myers C. Fluid resuscitation. Eur J Emerg Med 1997;4:224–32. 16. Hess JR, Holcomb JB, Hoyt DB. Damage control resuscitation: The need for specific blood products to treat the coagulopathy of trauma. Transfusion 2006;46(5):685–6. 17. Surgical management of penetrating brain injury. J Trauma 2001;51:S16–25. In: Prognosis in penetrating brain injury. J Trauma 2001;(2). Supplement. 18. Coupland RM, PP. Craniocerebral war wounds: Non specialist management. Injury 1992;23:21–4. 19. Spalding TJW, Stewart MPM, Tulloch DN, Stephens KM. Penetrating missile injuries in the Gulf war 1991. Br J Surg 1991;78:1102–4. 20. Adley R, Evans DHC, Mahoney PF, et al. The Gulf war: Anaesthetic experience at 32 Field Hospital Department of Anesthesia and Resuscitation. Anaesthesia 1992;42:996–9. 21. Page RJE, Wilson IH. Draw over anesthesia. Br J Hosp Med 1989;42:320–4. 22. Craig GR, Berry CB, Yeats MJ. An evaluation of the Universal PAC and the Oxford Miniature Vaporizers for paediatric field anaesthesia. Anaesthesia 1995;50:789–93. 23. Houghton IT. The Triservice anaesthetic apparatus. Anaesthesia 1981;36:1094–108.

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24. Brock-Utne JG. Anaesthesia in military conflicts: Towards simpler, safer and higher standards. Mil Med 1992;157: 229–30. 25. Knight RJ, Houghton IT. Field experience with the Triservice anaesthetic apparatus in Oman and Northern Ireland. Anaesthesia 1981;36:1122–27. 26. Jowitt MD, Knight RJ. Anaesthesia during the Falklands campaign: The land battles. Anaesthesia 1983;38:776–83. 27. Roberts MJ, Bell GT, Wong LSS. The CompPAC and PortaPAC Portable ventilators. Bench tests and field experience. J R Army Med Corps 1999;145:73–7. 28. Halford FJ. A critique of intravenous anaesthesia in war surgery. Anaesthesiology 1943;4:67–9. 29. Adams RC, Gray HK. Intravenous anaesthesia with pentothal sodium in the care of gunshot wounds associated with accompanying severe traumatic shock and loss of blood: Report of a case. Anaesthesiology 1943;4:70–3. 30. Editorial: The question of intravenous anaesthesia in war surgery. Anaesthesiology 1943;4:74–7. 31. Bennetts FE. Thiopentone anaesthesia at Pearl Harbor. Br JAnaesth 1995;75:366–8. 32. Restall J, Tully AM, Ward PJ, Kidd AG. Total intravenous anaesthesia for military surgery. A technique using ketamine, midazolam and vecuronium. Anaesthesia 1988;43:46–9. 33. Bailie R, Craig G, Restall J. Total intravenous anaesthesia for laparoscopy. Anaesthesia 1989;44:60–3. 34. Wilson RJT, Ridley SA. The use of propofol and alfentanil by infusion in military anaesthesia. Anaesthesia 1992;47:231–3. 35. Restall J, Thompson MC, Johnston IG, Fenton TC. Anaesthesia in the field. Spontaneous ventilation – a new technique. Anaesthesia 1990;45:965–8. 36. Smith C, McEwan E, Jhaveri R, et al. The interaction of fentanyl on the CP50 of propofol for loss of consciousness and skin incision. Anesthesiology 1994;81:820–8. 37. Vuyk J, Lim T, Engbers FHM, et al. The pharmacodynamic interaction of propofol and alfentanil during lower abdominal surgery in female patients. Anesthesiology 1995;83:8–22. 38. Vuyk J, Mertens MJ, Olofsen E, et al. Propofol anesthesia and rational opioid selection: Determination of optimal EC50EC95 propofol-opioid concentrations that assure adequate anesthesia and a rapid return of consciousness. Anesthesiology 1997;87:1549–62. 39. Badrinath S, Avramov MN, Shadrick M, et al. The use of ketamine-propofol combination during monitored anesthesia care. Anesth Analg 2000;90:858–62. 40. Fu ES, Miguel R, Scharf JE. Preemptive ketamine decreases postoperative narcotic requirements in patients undergoing abdominal surgery. Anesth Analg 1997;84:1086–90. 41. Guillou N, Tanguy M, Seguin P, et al. The effects of smalldose ketamine on morphine consumption in surgical intensive care unit patients after major abdominal surgery. Anesth Analg 2003;97:843–7. 42. Menigaux C, Fletcher D, Dupont X, et al. The benefits of intraoperative small-dose ketamine on postoperative pain after anterior cruciate ligament repair. Anesth Analg 2000;90:129–35. 43. Menigaux C, Guignard B, Fletcher D, et al. Intraoperative small-dose ketamine enhances analgesia after outpatient knee arthroscopy. Anesth Analg 2001;93:606–12. 44. Suzuki M, Tsueda K, Lansing PS, et al. Small-dose ketamine enhances morphine-induced analgesia after outpatient surgery. Anesth Analg 1999;89:98–103.

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45. Weinbroum AA. A single small dose of postoperative ketamine provides rapid and sustained improvement in morphine analgesia in the presence of morphine-resistant pain. Anesth Analg 2003;96:789–95. 46. Reich DL, Silvay G. Ketamine: an update on the first twenty five years of clinical experience. Can J Anaesth 1989;36: 186–97. 47. Hirota K, Lambert DG. Ketamine: Its mechanism(s) of action and unusual clinical uses. Br J Anaesth 1996;77: 441–4. 48. Pederson L, Benumof J. Incidence and magnitude of hypoxemia with ketamine in a rural African hospital. Anaesthesia 1993;48:67–9. 49. Drummond GB. Comparison of sedation with midazolam and ketamine: Effects on airway muscle activity. Br J Anaesth 1996;76:663–7. 50. Ketamine – a new anaesthetic (Editorial). Br Med J. 1971 June 19;2(5763):666–667. 51. Kerz T, Dick WF. Analgesia and sedatives in emergencies. In Goris RJA, Trentz O, ed. The Integrated Approach to Trauma Care: The First 24 Hours. Berlin: Springer-Verlag, 1995. 52. Mortero RF, Clark LD, Tolan MM, et al. The effects of smalldose ketamine on propofol sedation: respiration, postoperative mood, perception, cognition, and pain. Anesth Analg 2001;92: 1465–9. 53. White PF, Ham J, Way WL, Trevor AJ. Pharmacology of ketamine isomers in surgical patients. Anesthesiology 1980;52: 231–9. 54. Kloss T, Lenz G, Schwandt-Boden H, Bauer J, Stehle R. The role of regional anaesthesia under field conditions. Prehospital and disaster medicine (1990) 5(4):349–52. 55. Bion JF. Isobaric bupivacaine for spinal anaesthesia in acute war injuries. Anaesthesia 1984;39:554–9. 56. Bacon DR, Lema MJ. Standing on the promises: The career of Samuel L. Lieberman, M.D. Sphere 1989;42:20–4. 57. Thompson GE. Anesthesia for battle casualties in Vietnam. JAMA 1967;201:215–9. 58. Jenicek JA, Perry LB, Thompson GE. Armed forces anesthesiology comes of age. Anesth Analg 1967;46:822–32. 59. Lenz G, Stehle R. Anaesthesia under field conditions. A review of 945 cases. Acta Anaesthesiol Scand 1984;28:351–6. 60. Plunkett AR, Brown, DS, Rogers JM, Buckenmaier CC III. Supraclavicular continuous peripheral nerve block in a wounded soldier: When ultrasound is the only option. Br J Anaesth 2006;97(5):715–17. 61. Horlocker TT, Wedel DJ, Benzon H, et al. Regional Anesthesia in the Anticoagulated Patient: Defining the Risks. (The Second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation April 25–28, 2002. Available at: www.asra.com/consensus-statements). Reg Anesth Pain Med 2003;28:172–97. 62. Isenbarger DW, Atwood JE, Scott PT, et al. Venous thromboembolism among United States soldiers deployed to Southwest Asia. Thromb Res 2006;117(4):379–83. 63. Buckenmaier CC III, Shields CH, Auton AA, et al. Continuous peripheral nerve block in combat casualties receiving lowmolecular weight heparin. Br J Anaesth 2006;97(6):874–7. 64. Pesonen P. Pulse oximetry during ketamine anaesthesia in war conditions. Can J Anaesth 1991;38(5):592–4.

65. Bowdle TA, et al. Psychedelic effects of ketamine in healthy volunteers: Relationship to steady-state plasma concentrations. Anesthesiology 1998;88:82–8. 66. Strebel S, et al. Effects of ketamine on cerebral blood flow velocity in humans. Anaesthesia 1995;50:223–8. 67. Albanese J, et al. Ketamine decreases intracranial pressure and elecroencephalographic activity in traumatic brain injury patients during propofol sedation. Anesthesiology 1997;87: 1328–34. 68. Saegusa K, et al. Pharmacologic analysis of ketamine-induced cardiac actions in isolated, blood-perfused canine atria. J Cardiovasc Pharmacol 1986;8:414–9. 69. Gelissen HP, et al. Inotropic effects of propofol, thiopental, midazolam, etomidate, and ketamine on isolated human atrial muscle. Anesthesiology 1996;84:397–403. 70. Doenicke A, et al. The action of S(+)-ketamine on serum catecholamine and cortisol. A comparison with ketamine racemate. Anaesthesist 1992;41:597–603. 71. Nakayama M, Murray P. Ketamine preserves and propofol potentiates hypoxic pulmonary vasoconstriction compared with the conscious state in chronically instrumented dogs. Anesthesiology 1999;91:760–71. 72. Katz RI, et al. Hemodynamic stability and patient satisfaction after anesthetic induction with thiopental sodium, ketamine, thiopental-fentanyl, and ketamine-fentanyl. J Clin Anesth 1993;5:134–40. 73. Frizelle HP, et al. A comparison of propofol with a propofolketamine combination for sedation during spinal anesthesia. Anesth Analg 1997;84:1318–22. 74. Ikeda T, et al. Induction of anesthesia with ketamine reduces the magnitude of redistribution hypothermia. Anesth Analg 2001;93:934–8. 75. Engelhard K, et al. The effect of the [alpha]2-agonist dexmedetomidine and the N-methyl-d-aspartate antagonist S(+)-ketamine on the expression of apoptosis-regulating proteins after incomplete cerebral ischemia and reperfusion in rats. Anesth Analg 2003;96:524–31. 76. Kissin I, et al. The effect of ketamine on opioid-induced acute tolerance: can it explain reduction of opioid consumption with ketamine-opioid analgesic combinations? Anesth Analg 2000;91:1483–8. 77. Hill GE, et al. ketamine inhibits the proinflammatory cytokineinduced reduction of cardiac intracellular cAMP accumulation. Anesth Analg 1998;87:1015–9. 78. Van der Linden, et al. Comparison of halothane, isoflurane, alfentanil, and ketamine in experimental septic shock. Anesth Analg 1990;70:608–17. 79. Mahoney PF, Steinbruner D, Mazur B, Dodson C, Mehta SG. Management of c spine injury in combat casualties. Injury 2007;38:1220–2. 80. United States Army Institute of Surgical Research. Fort Sam Houston, Texas. http://www.usaisr.amedd.army.mil/. 81. Malchow, RJ. Ultrasonography in Advanced Regional Anesthesia and Acute Pain Management in a Combat Environment, Randall J. Malchow, MD, COL, MC, U.S. Army, Staff Anesthesiologist, 47th Combat Support Hospital, Mosul, Iraq. (Document in preparation.) 82. Second Consensus Conference on Neuraxial and Anticoagulation, April 25–28, 2002.

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SOURCE DOCUMENTS

Cantelo R, Mahoney PF. An introduction to field anaesthesia. Curr Anaesth Crit Care 2003;14:126–30.

Elements of this chapter draw on previously published work, which includes:

The sources above are used with permission of Elsevier.

Brooks A, Wood P, Mahoney P. Field resuscitation. Curr Anaesth Crit Care 2002;13:256–60. Clasper JC, Jeffrey PA, Mahoney PF. The forward deployment of surgical teams. Curr Anaesth Crit Care 2003;14:122–5.

Wood PR, Brooks AJ, Mahoney PF. Resuscitation and anaesthesia for the ballistic casualty. In Mahoney PF, Ryan JM, Brooks AJ, Schwab CW, ed. Ballistic Trauma – A Practical Guide, 2nd edition. Berlin: Springer-Verlag, 2005, pp 151–67. The source above is used with permission of Springer-Verlag.

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Martin Dauber and Steven Roth Objectives 1. Define the basic anatomic and physiologic concepts of ocular trauma. 2. Review the anesthetic implications of eye injuries, including blindness following major surgery. 3. Evaluate the use of succinylcholine in patients with open-globe injuries.

INTRODUCTION Trauma to the eyes and resulting blindness can have life-altering impact. This chapter will present the implications for the anesthesiologist of trauma to the eye. Ocular trauma and basic anatomic and physiologic concepts will be defined and the incidence of these potentially devastating injuries will be reviewed. Anesthetic implications, including the timing of surgery, anesthetic drug selection, and other perianesthetic concerns will be addressed. The use of succinylcholine in patients with openglobe injuries is a long-standing controversy that we will discuss. Blindness following major trauma and resuscitation has significant implications for physicians caring for trauma patients.

DEFINITION A standard terminology for eye injury that has been adopted in the United States and internationally is known as the Birmingham Eye Trauma Terminology (BETT; Figure 23.1). The entire globe is considered, and the BETT is unambiguous, consistent, and simple to use. The definitions it provides will be utilized in this chapter. The BETT system clearly defines all injuries and places each type of injury within a comprehensive system of the whole eyeball [1]. The eye wall is defined as the cornea and the sclera. A full-thickness wound of these layers is an “open-globe” injury, whereas a “closed-globe” injury does not involve a full-thickness wound (Figure 23.2, see also color plate after p. 294). Mechanisms of injury are contusion, laceration, or rupture. Contusions can occur by direct delivery of energy (e.g., choroidal rupture) or through changes in the shape of the globe (e.g., angle recession) [2]. Because the eye is filled with vitreous, an incompressible liquid, an impact will increase the intraocular

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pressure (IOP), assuming the globe is intact. If vitreous or anterior chamber contents leak out, the eye is decompressed. The eye wall will rupture at its weakest point, such as the point of impact and dehiscence or a previously surgically sutured site. The actual wound, therefore, is produced by an insideout mechanism, whereas, in lacerations of the full-thickness of the eye wall caused by sharp objects, the result is an outside-in mechanism of injury.

INCIDENCE Eye trauma is a significant and disabling health problem in the United States where approximately 2.5 million injuries occur annually [2]. The National Institute for Occupational Safety and Health indicate that between 600,000 and 700,000 work-related eye injuries occur annually, with the construction industry at the highest risk [3]. An ocular foreign body is the most common type of injury, accounting for one-third of cases. Open wounds and contusions make up one-fourth of all work-related ocular injuries. Chemical, thermal, and radiation burns constitute the remaining eye injuries. This chapter will deal primarily with mechanical trauma to the eye, as the other injuries rarely present to the operating room. There are approximately 40,000 eye injuries related to sports annually in the United States, most occurring in children and young adults. Prevention of almost all of these injuries and the resultant blindness would be possible if proper eye protection were employed. Masks and eye guards are available for baseball, football, basketball, soccer, racquetball, and other sports, and are required by certain sports agencies (Figure 23.3, see also color plate after p. 294) [4]. These lenses are made from polycarbonates and should bear the approval of the American Society for Testing and Materials (ASTM).

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Open globe

Closed globe

Lamellar laceration

Penetrating

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Injury

Contusion

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IOFB

Rapture

Perforating

Figure 23.1. The Birmingham Eye Trauma Terminology System (BETTS). The double-framed boxes show the diagnoses employed in clinical practice. IOFB, intraocular foreign body.

Figure 23.2. Conjunctival laceration with subconjunctival hemorrhage. This is an example of a closed-eye injury.

The location of the eye within the bony orbit results in frequent associated injuries to the head and neck. These other injuries include traumatic brain injuries, opened and closed, as well as cervical spine trauma with and without neurologic compromise (see Chapters 11–14). Because these associated injuries potentially have profound physiologic and prognostic implications, as well as a great impact on anesthetic plans, they must be addressed prior to ophthalmologic intervention. Nonetheless, early and thorough examination of the eyes should be accomplished to the greatest extent possible, preferably by an ophthalmologist skilled in ocular trauma care. Ophthalmologic Evaluation Patients who are suspected of having sustained orbital or periorbital/facial trauma must undergo a complete ophthalmologic evaluation after initial stabilization and evaluation. The extent of soft tissue and intraocular injury and bony disruption must be assessed. Acute or progressive loss of the visual axis from corneal opacification, cataract formation, or intraocular bleeding can inhibit complete ophthalmologic examination within a short time and may prevent appropriate diagnosis. The exam by the ophthalmologist will include assessment of visual acuity, papillary condition and function, motility of the eye, and intraocular pressure. Anterior segment evaluation with a slit lamp or handheld lens and funduscopic inspection of the posterior segment will be performed on the trauma patient as well. If penetrating injury to the globe is present, further examination will be limited so the globe can be shielded to prevent further extrusion of intraocular contents. If necessary, antiemetics such as metoclopramide, serotonin antagonists, or promethazine can be administered early to prevent vomitinginduced elevations in IOP. Transdermal scopolamine ought to be avoided as it may blur vision and confuse ophthalmologic diagnosis. In many reviews, prediction of a favorable visual outcome from ruptured globes included visual acuity of 20/200 on admission, rupture anterior to the insertion of the rectus muscles, length less than 1.0 cm, and a sharp mechanism of injury [5, 6]. Predictors of poor visual outcome include visual acuity no better than light perception, wounds extending posterior to the recti or longer than 1.0 cm, or a blunt mechanism of injury. Aggressive surgical management may, nonetheless, be undertaken in these high-risk patients to prevent visual loss. Intraocular pressure is the issue most important to the anesthesiologist, after the possibility of visual salvage has been ascertained. In trauma patients, the IOP is important at either high or low values. Extremely low pressures may indicate occult globe penetration, although this is by no means pathognomonic, as the IOP may be low, high, or normal in the case of a ruptured globe. Extremely high pressure may indicate retrobulbar hemorrhage that may be a harbinger of central retinal arterial occlusion or optic nerve damage. Either elevated or depressed IOP may cause pain and nausea. Pediatric Considerations

Figure 23.3. An open-eye injury resulting from trauma from a racquet.

Most of the considerations regarding adult ocular trauma patients are the same in children, but there are recognizable

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differences regarding epidemiology, as mentioned before, the timing of repair of fractures, and the impact these repairs may have on the growth of the child. Craniofacial anatomical differences in children under seven years of age make them more susceptible to orbital roof fractures. These fractures rarely require surgical intervention, in contrast to other orbital and midface fractures [7]. The difference in incidence may be due to the increased craniofacial ratio in infants, lower facial bone density and thickness, and underdeveloped paranasal sinuses. Children are thus less likely to present for emergency anesthesia for orbital fractures.

Aqueous humor Conjunctiva Cornea

Lens

Timing of Surgery The ophthalmologist’s evaluation will presumably lead to a rational surgical or nonsurgical plan based both on the eye findings and on the overall condition of the patient. In polytrauma patients, ocular interventions are typically postponed unless other injuries are not severe and visual salvage is possible. In unstable patients, regardless of the ophthalmologic imperative or likely visual prognosis, delay of eye surgery is necessarily indicated. In patients without life-threatening or other major trauma, the timing of ophthalmologic surgery needs to be determined by the need for urgent versus delayed surgery. Delay of surgery is preferred if the risk of visual loss is not thereby increased. Further medical evaluation of both trauma-related issues (e.g., central nervous system and cervical spine injuries) and coexisting medical disease can occur during the interval between the trauma and the surgery. Also, if ophthalmologic intervention is delayed, “full-stomach” status may be improved, or, at the very least, antiacid and antireflux prophylaxis can be administered and begin to exert their pharmacologic effects, to decrease the risk from aspiration of gastric contents. The determination by the ophthalmologist of the possibility of vision salvage or the certainty of full visual loss must enter into the consideration of the need for emergency anesthesia. In the absence of other injuries that require immediate induction of general anesthesia, the risks of emergency anesthesia in the unprepared patient must be balanced against the potential benefit of ophthalmologic intervention. Additionally, many injuries to the eye, especially those to the external tissues (eyelid, conjunctiva, cornea, and iris) may be treated medically or under local or topical anesthesia in the emergency department rather than in the operating room. If the patient is anesthetized for treatment of other injuries in any case, however, the ophthalmologist may choose to treat the eye injuries under the general anesthetic. Intraocular Pressure A thorough understanding of the concept of IOP is beyond the scope of this chapter, although some basic concepts will be reviewed. A comprehensive discussion of this topic for anesthesiologists is available in a chapter authored by Doctors McGoldrick and Gayer [7a]. It is the balance between production and elimination of the aqueous humor that maintains the IOP (Figure 23.4). Two thirds of this liquid humor is produced by the ciliary bodies through the mechanism of active secretion. This process is modulated by both the carbonic anhydrase and cytochrome oxidase systems. The remaining third is produced by passive filtration in the anterior surface of the iris. Drainage occurs via the trabec-

Anterior chamber

Iris Posterior chamber Trabecular meshwork Canal of Schlemm Sclera Ciliary body

Figure 23.4. Diagram of the flow of aqueous humor in the eye.

ular network, the canal of Schlemm, and the episcleral vessels [8]. Maintenance of IOP within the normal range of 10–20 mmHg is important for ocular homeostasis. Pressures greater than 22 mmHg are considered abnormal, and prolonged elevations of IOP can lead to permanent visual loss,. The IOP may be 1–6 mmHg higher while the patient is supine rather than sitting upright, which is the typical position for patients during ophthalmologic examination. As in any semiclosed system, the factors that may influence and alter IOP include external, internal, and wall tension. In trauma patients, the condition of the extraocular muscles, bony injuries around the orbit, retching or vomiting, and iatrogenic manipulations all may affect external compression. Rupture of the globe causing extrusion of contents or hemorrhage into the globe as a result of blunt trauma can influence the internal contribution to IOP. Succinylcholine and the Eye Succinylcholine remains the only depolarizing neuromuscular blocker available for clinical use. Its rapid onset, short duration, and long history of clinical experience make it a preferred drug for rapid sequence intubation in the trauma patient (see Chapter 9). Despite some undesirable adverse effects, succinylcholine remains an integral option in the anesthetic plans of many emergency patients. It exerts presynaptic, postsynaptic, and extrajunctional effects. Clinically, succinylcholine depresses the height of a single twitch and facilitates endotracheal intubation. The publication in the general medical literature of the potential role that succinylcholine could play in anesthesia practice occurred in 1952 [9]. The following year it was reported

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in Europe that succinylcholine measurably increased IOP [10]. The American literature then followed with the publication of several anecdotes from ophthalmologists that exudation of vitreous occurred after patients received succinylcholine [11]. It was suggested in the anesthesia literature that this loss of vitreous occurred when succinylcholine was given under “light anesthesia” conditions. It was stated that the use of succinylcholine in intraocular surgery was “hazardous” [12]. This reputation has persisted in many forms since that time. In a 1986 retrospective review of the experience at the Wills Eye Hospital of open-eye trauma patients, 81 percent of patients underwent general anesthesia. Eighty-eight percent of those underwent an intravenous induction, 90 percent of whom received succinylcholine. The remainder, all of whom were children, had an inhalation induction. Operative reports were reviewed in detail as were progress notes from the postoperative period. No extrusion of vitreous was noted in any patient who had received succinylcholine. In addition, the authors noted in their discussion that they were not aware of any anecdotal reports from Wills Eye Hospital of loss of eye contents in eye trauma patients over the prior decade [13]. Case reports of succinylcholine-induced vitreous extrusion followed, as did other institutional anecdotes of the reported ocular safety of succinylcholine [14, 15]. Scientific study of the effects of succinylcholine on the open globe followed these reports. Intraocular pressure increases in humans one minute after succinylcholine administration, and peaks at an elevation of 9 mmHg within 6 minutes. Many mechanisms have been proposed for this increase, including the contraction of extraocular muscles in response to succinylcholine forcing globe contents out of the orbit. A cat model, however, did not substantiate this theory [16]. An elegant study in humans undergoing enucleation under general anesthesia demonstrated that the increase in IOP after succinylcholine occurs even after detachment of all of the extraocular muscles [17]. The current theory for the succinylcholine-induced elevation in IOP is related to a vascular mechanism, whereby either choroidal vascular dilatation or decrease in vitreous drainage as a result of elevated central venous pressure (causing an increase in resistance to outflow) decreases drainage of vitreous through the canal of Schlemm [18]. Several techniques have been advocated for the blunting of the elevation in IOP from succinylcholine. Included among them are “self-taming,” defasciculating with nondepolarizing relaxants, and other pharmacologic pretreatment. Self-taming implies the administration of a small, subclinical dose of succinylcholine (0.2 mg/kg in this study) one minute prior to the rapid sequence intubating dose. This has been shown to be ineffective and, in fact, the IOP rises in response to the small dose [19]. Lidocaine (intravenous dose of 1 mg/kg) blunts the increase caused by succinylcholine and further blunts the rise in IOP seen with endotracheal intubation, though d-tubocurare and diazepam provide neither benefit [20]. All of the opiates commonly used in clinical anesthesia, including fentanyl, alfentanil, sufentanil, and remifentanil, have been shown to blunt the IOP elevation following succinylcholine and intubation [21– 23]. Nifidipine, nitroglycerin, propranolol, and clonidine all exert protective effects on IOP, but may be contraindicated in the polytrauma patient [24–26]. Note that these studies were all done in elective surgical patients without eye injuries and with intact globes.

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It is clear that succinylcholine does indeed increase IOP. However, during the period surrounding the induction of anesthesia, there are many factors that also change IOP. These include supine positioning, coughing, retching, Valsalva maneuvers, or crying. In addition, mask ventilation with compression of the orbit while awaiting paralysis from the sloweronset nondepolarizing neuromuscular relaxants will directly elevate IOP. Coughing during intubation from any cause will also adversely affect IOP and is to be avoided. Airway assessment combined with ophthalmologic impressions need to be discussed by the anesthesia and ophthalmology teams. Maintenance of ventilation is essential to all plans, independent of ocular implications. If rapid sequence induction and intubation is deemed appropriate, propofol, thiopental, opiates, and other drugs have been shown to minimize the effect of succinylcholine on IOP. If difficult tracheal intubation is anticipated, a determination of the viability of the eye is critical: If vision is not to be preserved, awake intubation can be selected (see Chapter 2). If the possibility of restoration or salvage of vision exists, IOP elevation will need to be avoided prior to any intubation sequence. In light of the benefits of succinylcholine for facilitating intubation as part of the standard rapid sequence induction of anesthesia in the full-stomach patient, its clinical use should not be limited. The main point is that, in the situation of an open-eye injury, the patient needs to be deeply anesthetized and immobile. How to do that is a matter of individual preference and should be tailored according to the patient’s needs and the anesthesiologist’s preferences. Ischemic Optic Neuropathy (ION) Ischemic optic neuropathy, the leading cause of sudden visual loss in patients 50 years of age or older, primarily occurs spontaneously without warning signs, and rarely is found in the setting of non-ocular surgery. There are two types of ION: anterior (AION) and posterior (PION). Of the two, AION is far more common in the overall population and has been more extensively studied than PION. ION has been found after a wide variety of surgical procedures, with the majority having followed cardiothoracic [27–29], instrumented spinal fusion operations [30, 31], head and neck surgery [32], and surgery on the nose or sinuses [33, 34]. However, cases have also been described after vascular surgery, general surgical, and urologic procedures, cesarean delivery, gynecologic surgery, and liposuction [35–40]. With advances in trauma resuscitation, patients who would have died before are surviving, and the incidence of ION and the resultant blindness is likely to increase in these patients. C U R R E N T K N OW L E D G E A N D C O N T ROV E R S I E S Perioperative ION appears to be a multifactorial disease, and unlike spontaneously occurring ION, it can occur in younger patients. Because there are few case-controlled studies and no prospective studies, the risk factors have not yet been well defined [41]. Another puzzling feature of this dreaded complication is that it is unclear why some patients develop AION and others develop PION. Some possible factors involved in

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the etiology of perioperative ION are common in multiple trauma patients and include decreased systemic blood pressure, large blood loss, increased intraocular or orbital venous pressure, abnormal autoregulation of the optic nerve circulation and/or anatomic variation in the blood supply to the optic nerve, emboli, use of vasopressors, the presence of systemic diseases such as hypertension, diabetes, and atherosclerosis, and retrobulbar hemorrhage. It seems that one or more of these factors are often involved in an individual patient and in an unpredictable fashion. Intraoperative hypotension has been cited as an important risk factor by a number of authors of case reports [36, 42, 43], but it is not always present, suggesting that hypotension itself might not be responsible. Hypotension can potentially lead to decreases in perfusion pressure in the optic nerve. The anterior optic nerve would be susceptible to damage from hypotension leading to AION either because of anatomical variation in the circulation or because of abnormal autoregulation and inability to adequately compensate for a decrease in perfusion pressure. The posterior optic nerve would be at potential risk leading to PION because of the relatively limited blood supply reaching this area, which might be potentiated by hypotension. It is difficult to precisely define the degree of hypotension that is potentially harmful, as actual pre- and intraoperative blood pressures were not available in many of the reported cases of ION in the literature, and hence the safe “lower limits” of blood pressure are not known. From case reports of perioperative ION, it is apparent that, on average, patients sustained considerable blood loss and had decreased hemoglobin concentration intraoperatively. Routine clinical practice based on the National Institutes of Health (NIH) Consensus Panel on Blood Transfusion [46] and American Society of Anesthesiologists (ASA) practice guidelines [47] indicate that transfusion is generally not required for hemoglobin values greater than 8.0 g/dL (see Chapter 6). A number of authors have suggested that allowing hemoglobin to decrease to such low values may be putting patients at increased risk for ION; [36, 48] however, whether practice should be changed in surgical procedures for major trauma surgery remains controversial. In the setting of uncontrolled hemorrhage, where blood volume is not maintained, decreased oxygen delivery to the optic nerve could result in either AION or PION [49, 50]. Just how low or for low long hemoglobin concentration must decrease to lead to this complication is not known. However, the presence of recurrent and profound hemorrhage has been described in many reports. The effects of combined hypotension and hemodilution on hemodynamics and O2 delivery in the optic nerve have not been studied but remain a concern. Intraocular Pressure Changes and Venous Hemodynamics in the Eye AION and PION have been reported in the setting of massive fluid replacement, and many reports include patients that were operated on in the prone position. This raises the possibility that either external pressure on the globe or a build-up of pressure internally within the eye could be related to ION. It is unlikely that PION is related to external pressure because the retrolaminar optic nerve is not exposed to the IOP. In addition, an increase in IOP would not be likely to produce an

isolated ION without also causing retinal damage, because sustained increases in IOP significantly decrease both retinal and choroidal blood flows [51]. The theory that massive fluid resuscitation could be a pathogenic factor in perioperative ION remains speculative, but does have some merit. Conceivably, fluid therapy could result in increased IOP, and/or accumulation of fluid in the optic nerve. Because the vessels in the optic nerve are small and relatively easily compressed, especially in the posterior optic nerve, largevolume replacement might lead to decreased arterial supply, or increased orbital venous pressure and the risk of venous stasis. Because the central retinal vein and draining veins exit out of the optic nerve, it is possible that an “internal compartmental syndrome” may occur in the optic nerve. In a remarkable report, Cullinane et al. [52] found that 2.6 percent of trauma patients who were resuscitated successfully by using more than 20 L of crystalloid in a 24-hour period developed ION. Patients were said, in this publication, to have sustained AION, but from the ocular findings reported, it appears the diagnosis was in fact PION. These patients received massive blood replacement and were acidotic, most had abdominal compartmental syndrome, and the lowest hematocrit ranged from 7.5 to 28 percent. Also, very high levels of positive end-expiratory pressure (PEEP) (average, 29 cm) were used to ventilate these patients. Although there are many complicating factors in these patients, massive fluid and blood replacement seem likely as possible etiologic factors for ION. Vasopressors Hayreh theorized that AION is related to excessive secretion of vasoconstrictors, which could in turn lower optic nerve perfusion to dangerously low levels [50, 52]. Clinicians often use vasopressors to maintain blood pressure, especially after cardiac surgery. Shapira et al. showed an association between prolonged use of epinephrine or long bypass time and ION in patients undergoing open heart surgery [27]. Lee and Lam reported a case of ION in a patient after lumbar spine fusion during which a phenylephrine infusion was used to maintain blood pressure [45]. However, these reports cannot distinguish whether vasopressors altered hemodynamics in the optic nerve or if the use of vasopressors represents a marker for patients with profound systemic abnormalities. Prognosis and Treatment Unfortunately, there is no proved treatment of ION. Williams et al. [48] have reviewed the attempted treatments. Acetazolamide lowers IOP and may improve flow to the optic nerve and retina [53, 54]. Diuretics such as mannitol or furosemide reduce edema. In the acute phase, corticosteroids may reduce axonal swelling, but in the postoperative period they increase the risk of wound infection. Because steroids are of unproved benefit, their use must be carefully weighed. Increasing ocular perfusion pressure or hemoglobin concentration may be appropriate when ION occurs in conjunction with significant decreases in blood pressure and hemoglobin concentration. Maintaining head-up position could be valuable if increased ocular venous pressure is suspected. Similarly, IOP should be lowered if an increase is documented. Optic nerve decompression is an operative procedure that could restore circulation in the optic nerve. However, in a multicenter trial sponsored by the National Eye Institute, this operation was found

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to be ineffective and possibly harmful; because of the adverse findings, this study was terminated prematurely [55]. Despite the devastating nature of ION, our limited understanding of the pathogenesis of this disorder, at this time, does not yet enable us to make rational recommendations that are likely to completely prevent its occurrence.

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a. Intraocular pressure increases to 50 mmHg within five minutes after administration of succinylcholine b. Causes contraction of extraocular muscles and extrusion of vitreous in cats c. Increased IOP may be due to choroidal vascular dilatation or decrease in vitreous drainage d. A small dose of succinylcholine (self-taming) is effective in blunting the rise in IOP

C O N C LU S I O N S Although typically not life-threatening in the terms that anesthesiologists usually consider, ocular trauma can have devastating consequences that alter lifestyle. Current evidence favors the judicious use of succinylcholine in trauma patients to facilitate rapid and ideal endotracheal intubation conditions when appropriate, and when maneuvers to prevent acute elevations in IOP are instituted. Ophthalmologic evaluation, treatment, and prognostication allow anesthetic management of these patients that can optimize the visual outcome while exerting the minimum necessary effects on the overall physiology of the trauma patient. Ischemic optic neuropathy is a devastating complication that may be found in the perioperative period in patients that have been successfully resuscitated from massive trauma. The etiology remains unclear but patients with visual deficit should be examined immediately by an ophthalmologist to determine cause and provide any possible treatment.


Questions 1–3: Match the following statements 1–3 with the best answer (a–e). 1. Ischemic optic neuropathy 2. Ocular foreign body 3. Open-globe injury a. Laceration of the globe from penetrating trauma b. Always associated with loss of vitreous and anterior eye chamber contents c. Full-thickness injury of the eye wall including cornea and sclera d. Leading cause of blindness in patients more than 50 years old e. Most common type of eye injury Questions 4–6: Choose the one best answer 4. Which of the following is associated with increased intraocular pressure? a. b. c. d. e.

Retching Coughing Crying Valsalva maneuver All of the above

5. Concerning succinylcholine and intraocular pressure (IOP), which are true?

ANSWERS

1. d 2. e

3. c 4. e

5. c

REFERENCES

1. Kuhn F, Morris R, Witherspoon CD. Birmingham Eye Trauma Terminology (BETT): terminology and classification of mechanical eye injuries. Ophthalmol Clin N Am. 2002;15(2):139–43. 2. National Society to Prevent Blindness. Vision Problems in the U.S. – Data Analysis, National Society to Prevent Blindness, Chicago, Illinois, 2002. 3. United States Consumer Product Safety Commission, Directorate for Epidemiology; National Injury Information Clearinghouse. National Electronic Injury Surveillance System. Product Summary Report. U.S. Consumer Product Safety Commission, Bethesda, Maryland, 2003. 4. Official Rules of Racquetball. USA Racquetball Association, September 2004. Available at: http://usra.org/Rulebook/tabid/ 839/Default.aspx. 5. Grove AS. Computerized tomography in management of orbital trauma. Ophthalmology 1982;89:433–40. 6. Harlan JB, Pieramici DJ. Evaluation of patients with ocular trauma. Ophthalmol Clin N Am 2002;15(2):153–61. 7. Koltai PJ, Amjad I, Meyer D, Feustel PJ. Orbital fractures in children. [Journal Article. Research Support, U.S.P.H.S.] Arch Otolaryngol Head Neck Surg 1995;121(12):1375–9. 7a. McGoldrick KE, Gayer S. Anesthesia and the eye. In: Clinical Anesthesia, fifth edition. Edited by Barash P, Cullen B, Stoelting R, Lippincott Williams and Wilkins, Philadelphia PA. 2006, pp 974–96. 8. Forrester JV, Dick AD, et al. The Eye: Basic Sciences in Practice. Philadelphia: WB Saunders, 2002. 9. Foldes FF, Menall PG, Borrego-Hinojosa JM. Succinylcholine: A new approach to muscular relaxation in anesthesiology. N Engl J Med 1952;247:596–600. 10. Hofman H, Holzer H, Bock J, et al. The effect of muscle relaxants on intraocular pressure. Klin Monatsbl Augenheilk 1953;123:1– 15. 11. Lincoff HA, Breinin GM, Devoe AG. The effect of succinylcholine on the extraocular muscles. Am J Ophthalmol 1957; 43:440–4. 12. Dillon JB, Sabawala P, Taylor DB, et al. Action of succinylcholine on eye muscles and intraocular pressure. Anesthesiology 1957;18:44–9. 13. Libonati MM, Leahy JJ, Ellison N. The use of succinylcholine in open eye surgery. Anesthesiology 1986;62:637–40. 14. Rich AL, Witherspoon CD, Morris RE, et al. Use of nondepolarizing anesthetic agents in penetrating ocular injuries. Anesthesiology 1986;65:108–9.

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15. Donlon JV. Succinylcholine and open eye injuries. Anesthesiology 1986;65:526–7. 16. Moreno RJ, Kloess P, Carlson DW. Effect of succinylcholine on the intraocular contents of open globes. Ophthalmology 1991;98:636–8. 17. Kelly RE, Dinner M, Turner LS, et al. Succinylcholine increases intraocular pressure in the human eye with the extraocular muscles detached. Anesthesiology 1993;79:948–52. 18. Metz HS, Venkatesh B. Succinylcholine and intraocular pressure. J Pediatr Ophthalmol Strabismus 1981;18:12–4. 19. Verma RS. “Self-Taming” of succinylcholine-induced fasciculations and intraocular pressure. Anesthesiology 1979;50: 245. 20. Mahajan RP, Grover VK, Munjal VP, et al. Double blind comparison of lidocaine, tubocurarine and diazepam pretreatment in modifying intraocular pressure increases. Can J Anaesth 1987;34(1):41–5. 21. Alexander R, Hill R, Lipham WJ, et al. Remifentanil prevents an increase in intraocular pressure after succinylcholine and tracheal intubation. Br J Anaesth 1998;81:606–7. 22. Georgiou M, Parlapani A, Argiriadou H, et al. Sufentanil or clonidine for blunting the increase in intraocular pressure during rapid-sequence induction. Eur J Anaesthesiol 2002;19(11); 819–22. 23. Sweeney J, Underhill S, Dowd T, et al. Modification by fentanyl and alfentanil of the intraocular pressure response to suxamthonium and tracheal intubation. Br J Anaesth 1989;63:688–91. 24. Indu B, Batra YK, Puri GD, et al. Nifidipine attenuates the intraocular pressure response to intubation following succinylcholine. Can J Anaesth 1989;36:269–72. 25. Mahajan RP, Grover VK, Sharma SL, et al. Intranasal nitroglycerine and intraocular pressure during general anesthesia. Anesth Analg 1988;67(7):631–6. 26. Cook JH, Feneck RO, Smith MB. Effect of pre-treatment with propranolol on intra-ocular pressure changes during induction of anesthesia. Eur J Anaesthesiol 1986;3(6):449–57. 27. Shapira OM, Kimmel WA, Lindsey PS, et al. Anterior ischemic optic neuropathy after open heart operations. Ann Thorac Surg 1996;61:660–6. 28. Shahian DM, Speert PK. Symptomatic visual deficits after open heart operations. Ann Thorac Surg 1989;48:275–9. 29. Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982;32:560–2. 30. Roth S, Thisted RA, Erickson JP, et al. Eye injuries after non ocular surgery: a study of 60,965 anesthetics from 1988 to 1992. Anesthesiology 1996;85:1020–7. 31. Roth S, Nunez R, Schreider BD. Visual loss after lumbar spine fusion. J Neurosurg Anesthesiol 1997;9:346–8. 32. Chutkow JG, Sharbrough FW, Riley FC. Blindness following simultaneous bilateral neck dissection. Mayo Clin Proc 1973;48:713–7. 33. Buus DR, Tse DT, Farris BK. Ophthalmic complications of sinus surgery. Ophthalmology 1990;97:612–9. 34. Maniglia AJ. Fatal and major complications secondary to nasal and sinus surgery. Laryngoscope 1989;99:276–83. 35. Warner ME, Warner MA, Garrity JA, et al. The fre-

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48. 49.

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51. 52.

53. 54.

55.

quency of perioperative vision loss. Anesth Analg 2001;93: 1417–21. Brown RH, Schauble JF, Miller NR. Anemia and hypotension as contributors to perioperative loss of vision. Anesthesiology 1994;80:222–6. Chun DB, Levin DK. Ischemic optic neuropathy after hemorrhage from a cornual ectopic gestation. Am J Obstet Gynecol 1997;177:1550–2. Gupta M, Puri P, Rennie IG. Anterior ischemic optic neuropathy after emergency caesarean section under epidural anesthesia. Acta Anaesthiol Scand 2002;46:751–2. Williams GC, Lee AG, Adler HL, et al. Bilateral anterior ischemic optic neuropathy and branch retinal artery occlusion after radical prostatectomy. J Urol 1999;162:1384–5. Minagar A, Schatz NJ, Glaser JS. Liposuction and ischemic optic neuropathy: case report and review of literature. J Neurol Sci 2000;181:132–6. Roth S. The effects of isovolumic hemodilution on ocular blood flow. Exp Eye Res 1992;55:59–63. Katz DM, Trobe JD, Cornblath WT, et al. Ischemic optic neuropathy after lumbar spine surgery. Arch Ophthalmol 1994;112:925–31. Lee AG. Ischemic optic neuropathy following lumbar spine surgery. J Neurosurg 1995;83:348–9. Roth S, Barach P. Post-operative visual loss: still no answers yet. Anesthesiology 2001;95:575–6. Lee LA, Lam AM. Unilateral blindness after prone lumbar surgery. Anesthesiology 2001;95:793–5. Anonymous. Consensus conference: perioperative red blood cell transfusion. JAMA 1988;260:2700–3. Anonymous. Practice guidelines for blood component therapy: A report by the American Society of Anesthesiologists Task Force on Blood Component Therapy. Anesthesiology 1996;84: 732–47. Williams EL, Hart WM, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995;80:1018–29. Roth S, Gillesberg I. Injuries to the visual system and other sense organs. In Benumof JL, Saidman LJ, ed. Anesthesia and Perioperative Complications, 2nd edition. St. Louis: Mosby, 1999, pp 377–408. Hayreh SS. Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. Ophthalmology 1987;94:1488–502. Roth S, Pietrzyk Z. Blood flow after retinal ischemia in cats. Invest Ophthalmol Vis Sci 1994;35:3209–17. Cullinane DC, Jenkins JM, Reddy S, et al. Anterior ischemic optic neuropathy: A complication after systemic inflammatory response syndrome. J Trauma 2000;48:381–7. Rassam SM, Patel V, Kohner EM. The effect of acetazolamide on the retinal circulation. Eye 1993;7:697–702. Hayreh SS. Anterior ischaemic optic neuropathy. III. Treatment, prophylaxis, and differential diagnosis. Br J Ophthalmol 1974;58:981–9. Anonymous. The Ischemic Optic Neuropathy Decompression Trial Research Group. Optic nerve decompression surgery for non-arteritic anterior ischemic optic neuropathy is not effective and may be harmful. JAMA 1995;273:625–32.

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Jocelyn Loy Objectives 1. Describe the differences between pediatric and adult trauma. 2. Explain the initial evaluation and management priorities in an injured pediatric patient. 3. Describe the developing physiologic and anatomical characteristics of infants and children. 4. Identify anatomical characteristics of the pediatric airway and describe the associated implications for airway management after trauma with potential cervical spine injury. 5. Describe fluid options and blood product resuscitation for a bleeding pediatric patient. 6. Explain the anesthetic considerations applicable to the care of an injured child, and how trauma influences the choice of medications and other elements of the anesthetic plan. 7. Describe the physiology and pharmacology of drugs used in the management of injured infants and children. 8. List alternatives available for the management of pediatric acute postoperative pain, and explain the advantages and disadvantages of each.

Trauma remains the leading cause of mortality and serious long-term morbidity in the pediatric population. A significant majority of pediatric trauma occurs in motor vehicle accidents. Injuries related to falls and sports comprise the second largest group. Other causes include drowning, child abuse, and burns. Falls from heights are most common in toddlers, while older children sustain more traumatic injuries from motor vehicle and bicycle accidents [1]. Homicide is the leading cause of traumatic death in infants, 50 percent occurring in the first four months after birth [2]. Pediatric injuries vary from minor and isolated, to severe, multiple, and potentially fatal, involving several organ systems. Evaluation and assessment of the pediatric trauma patient requires an efficient, organized, and systematic approach to properly identify, prioritize, and treat the most life-threatening injuries and to achieve a favorable outcome, with minimal to no long-term functional limitations. Management principles of pediatric trauma patients are similar to those of adults, but modified according to the age group of the child. Children are not just small adults. Their unique, developing psychologic, anatomic, and physiologic characteristics pose special challenges to anesthesiologists and the entire trauma care team. Optimal management of the pediatric trauma patient depends on adequate knowledge and understanding of these unique characteristics.

I N I T I A L A S S E S S M E N T A N D M A N AG E M E N T Primary Survey The main goal of the primary survey is to rapidly find all potentially life-threatening injuries to prioritize management for efficient resuscitation and achieve hemodynamic stability. This requires immediate assessment of the “ABCDEs” of the Advanced Trauma Life Support (ATLS) protocol and constant reevaluation of the adequacy of resuscitation strategies. Airway with C-Spine Control Evaluation of the airway in an injured child can be complex. Injury to the airway or nearby structures may distort normal anatomy and render mask ventilation and tracheal intubation difficult. Preexisting conditions that may complicate emergency airway management include congenital abnormalities, such as micrognathia (mandibular hypoplasia), macroglossia, and cleft palate and the presence of obstructive sleep apnea with or without obesity. Assessment of the airway for signs of airway compromise or obstruction takes priority. Inability to establish, maintain, and secure a patent airway for oxygenation and ventilation can lead to hypoxia, hypercarbia, bradycardia, and cardiac arrest. Inspection of the airway includes the face, mouth, mandible, nose, and neck. Look for edema, foreign bodies, secretions,

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A

B

Figure 24.1. A and B. In the supine position, due to a relatively large occiput, the neck of an infant or a young child is naturally flexed on the chest while the head may be additionally flexed on the neck. This may result in partial or significant airway obstruction in a sedated or obtunded infant or young child. (Source for Figure 24.1A: Courtesy of medical illustrator at MetroHealth Medical Center; Source for Figure 24.1B: Herzenberg JE, Hensinger RN, et al. Emergency transport and positioning of young children who have an injury of the cervical spine. The standard backboard may be hazardous. J Bone Joint Surg Am 1989;71-A(1):16, 24.1B.)

blood, loose or missing teeth, and fractures of the jaw, mandible, and cervical spine. Any trauma victim, especially one with a closed-head injury, is presumed, until proved otherwise, to have cervical spine (C-spine) injury and a full stomach. C-spine precautions should be maintained and techniques that minimize the risk of pulmonary aspiration should be taken at all times. The anesthesiologist may be called on to help with airway management in the emergency room or first encounter the child in the operating room; hence, knowledge and appreciation of the peculiarities of the pediatric airway is mandatory. Healthy neonates and young infants have large heads, including prominent occiputs relative to body size, so that, in the supine position, the infant neck is naturally flexed on the chest and the supine infant head may be flexed on the neck (Figure 24.1A and B) [3, 4]. This has several important implications. The natural head and neck flexion of the obtunded or sedated young infant often results in significant airway obstruction that may be relieved by gently lifting the chin up and forward (anteriorly) to slightly extend the head on the neck. Otherwise, an oral airway can be inserted with no relative movement of head and neck. In suspected C-spine injury, a more neutral, straight head and neck position should be achieved by placing a blanket or pad under the supine infant or young child’s torso (Figure 24.2A and B) [4, 5]. Direct laryngoscopy may be facilitated by some of this natural supine flexion of neck on chest, as only slight additional extension of head on neck may be needed to achieve a good “sniffing position” for optimal laryngeal visu-

alization. In general, in infants and young children, the pad belongs under the body, not under the head. Neonates and young infants are obligate nose breathers until three to five months of age so that any secretions or blood in their relatively narrow nasal passages can lead to airway obstruction. Furthermore, the supine, obtunded, or sedated young infant’s relatively large tongue tends to fall against the soft palate, epiglottis, and posterior pharyngeal wall resulting in upper airway obstruction and difficulty with mask ventilation and direct laryngoscopy for intubation. Insertion of an oral airway, with the aid of a tongue depressor if needed, helps relieve the obstruction. The most appropriate size oral airway for the child is one that is approximately as long as the distance from the child’s lips to the angle of the mandible. A good face mask seal should be achieved by holding the face mask with the fingers pressing on the mandible only, avoiding pressure on the soft tissues in the submandibular area. Pressure on the submandibular soft tissue may actually push the tongue onto the palate and pharyngeal wall leading to further airway obstruction in proportion to the amount of pressure applied. In infants, touch the bone, not the soft tissue. The larynx in infants and children is more cephalad, approximately at the level of the C3–C4 vertebrae in infants compared with the C5–C6 level in adults (Figure 24.3) [6]. This may give the impression that the infant larynx is more anterior during direct laryngoscopy. The hard, narrow, and more omega-shaped infant epiglottis is also angled more posteriorly

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A

B

Figure 24.2. A and B. A blanket or pad placed under the torso of a supine infant or young child will achieve a neutral, straight head and neck position. (Source for 24.2A: Courtesy of medical illustrator at MetroHealth Medical Center; Source for Figure 24.2B: Herzenberg JE, Hensinger RN, et al. Emergency transport and positioning of young children who have an injury of the cervical spine. The standard backboard may be hazardous. J Bone Joint Surg Am 1989; 71-A(1):21, Figure 6B.)

Prominent occiput

Tongue is disproportionately large in relation to mouth C3 C4 Tongue

Larynx is higher in neck Narrowest portion at cricoid ring

C3 C4 C5

Larynx

Figure 24.3. Differences between adult and pediatric airway. (Source: From Finucane BT. Principles of Airway Management. Philadelphia: FA Davis, 1988.)

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Table 24.1: Pediatric Endotracheal Tube Sizes

Table 24.2: Guidelines for Endotracheal Tube Size (millimeters)

Internal Diameter (mm) Age

Uncuffed ETT

Cuffed ETT

Premature infant (

Trauma Anesthesia

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Obstetric Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Anesthesia Emergencies

Cultural Trauma

Trauma Rehabilitation

Trauma Rehabilitation

Anesthesia and Uncommon Diseases

Pediatric Anesthesia 1999

Consciousness, Awareness, and Anesthesia

Complications of Regional Anesthesia

Molecular Bases of Anesthesia

Essential Clinical Anesthesia

Anesthesia in Cosmetic Surgery

Clinical Cases in Anesthesia

Essentials of Regional Anesthesia

Trauma Alert

Talking Trauma

Trauma Alert

Trauma Anesthesia

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Trauma

Obstetric Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Clinical Anesthesia

Anesthesia Emergencies

Cultural Trauma

Trauma Rehabilitation

Trauma Rehabilitation

Anesthesia and Uncommon Diseases

Pediatric Anesthesia 1999

Consciousness, Awareness, and Anesthesia

Complications of Regional Anesthesia

Molecular Bases of Anesthesia

Essential Clinical Anesthesia

Anesthesia in Cosmetic Surgery

Clinical Cases in Anesthesia

Essentials of Regional Anesthesia

Trauma Alert

Talking Trauma

Trauma Alert

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